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Muscular System Chapter 10 p.274 Introduction The bones provide the levers and structure of the skeleton but it is the muscles that cause the movement. Motion results from the contraction and relaxation of muscles. The muscles change chemical energy (ATP) into mechanical energy to generate force, perform work and produce movement.

• Muscles account for 40-50% of total body weight.

• The scientific study of muscles is known as myology. Functions of Muscle Tissue Muscle tissues have a specialized property- contractility, the capability of shortening. Through the contraction and relaxation of muscles, 4 functions can be described: Fig. 10.1 p276, p 274

1. Motion such as walking, running, grasping.

These movements rely on the integrated function of bones, joints, and skeletal muscles (as well as the nervous system). The muscles are connected to the skeleton and pull to cause movement. Mostly voluntary.

2. Propulsion of materials through the body (blood, ingested food, sperm, ova, urine).

Examples: Cardiac muscle contracts to pump blood to all body tissues.

Physiology 7 PhysiologyStudentNotes 2 1

Smooth muscle contractions aid in the movement of food through the GI tract, urine through urinary system. Skeletal muscle (squeezing upon contraction) helps return venous blood and lymph to the heart.

3. Maintain body posture and sphincter control.

Examples: Skeletal muscle (antagonistic) contractions maintain the body in stable positions as a when standing, an example of muscle tension without movement. Sustained contraction of smooth muscles (sphincters) prevent outflow of contents of a hollow organ, as in the urinary bladder, colon, or stomach.

4. Thermogenesis (generating heat).

Heat is a byproduct of muscle contraction. Muscle generates about 85% of body heat. Fig 10.11 p 251 When more heat is needed to maintain body temperature, involuntary muscle contraction (shivering), can increase thermogenesis by several 100%. Smooth muscle in arteriole wall will contract to conserve heat and relax to increase blood flow to the skin and remove heat from the body.

Contractile Proteins Movement in living cells involves special protein molecules, contractile proteins. Contractile proteins can convert chemical energy in ATP, into the mechanical energy of motion.


Surprisingly, contractile proteins have been found in many types of cells other than muscle cells. They account for things like:

1. Movement of chromosomes in cell division. 2. Movement of WBCs (and mitochondria). 3. Movement of cilia and flagella (as in sperm).

Therefore, muscle tissue is not unique in its possession of contractile proteins but muscle tissue is distinguished by its high concentration of contractile proteins. Types of Muscle Tissue p 274 There are 3 types of muscle tissue: 1. Skeletal muscle. 2. Smooth (visceral) muscle. 3. Cardiac muscle. Let's look at the 3 types of muscle tissue more closely.

1. Skeletal Muscle Is the muscle that is typically attached to the skeleton and is responsible for movement:

a. of the skeleton. b. of the diaphragm in breathing. c. Sphincters

Circles of skeletal muscle important in voluntary release of urine and feces.

• Contraction of skeletal muscle occurs by way of nerve

impulses. (somatic motor neurons). • You have voluntary control of the contraction of skeletal

muscle. Therefore sometimes called, voluntary muscle.


• Skeletal muscle is the largest tissue of the body, approximately 40% of body weight.

2. Smooth (visceral) muscle

• Visceral refers to internal organs of chest and abdomen.

• Smooth muscle surrounds the hollow tubes and chambers of the body.

• Found in organs of digestive system, reproductive, urinary, and blood vessels.

• Also found in skin attached to hair follicles.

• Smooth muscle functions to propel things through tubes (peristalsis = wave like contractions).

• May change size (diameter) of an organ, important in

maintaining proper blood flow and pressure. Do you have voluntary control over contraction of smooth muscle? No. Involuntary muscle. Contraction of smooth muscle is inherent (automatic or involuntary). There are several types of control vs. skeletal muscle. Contraction of smooth muscle may be altered by: p298-9

a. Physical stimulus: • Stretching initially causes contraction followed by

relaxation with continued tension on contents of tubing, so pressure remains constant. Allows tubing to lengthen while maintaining pressure. Called stress-relaxation response.

b. Chemicals c. Nerves (via neurotransmitters) creating action potentials

mainly from the Autonomic Nervous System (ANS). • Visceral muscle action potentials are spread to

neighboring muscle fibers thru gap junctions.


• In multiunit muscle tissue, only the muscle fibers touched by a nerve contract. Example: walls of larger arteries, airways, arrector pilli

d. Hormones • Examples: e.g. epinephrine from adrenal medulla relaxes

airways). e. Local changes (temperature, pH, O2, CO2).

3. Cardiac muscle

• Cardiac muscle is the muscle of the heart. • It serves to pump (propel) the blood. • Cardiac muscle contractions are inherent (originate in the

heart not nervous system) and includes a pacemaker that causes the heart to beat. Autorhythmic.

• The heart rate may be modulated by ANS nerves (neurotransmitters) and other chemicals (hormones: epinephrine and norepinephrine speed up, Ca++ strengthens contraction).

• Cardiac and smooth muscle together makeup about 10% of body weight.

Note: In this section we primarily will discuss skeletal muscle and to a lessor extent smooth muscle. We will discuss heart muscle further when we get to the cardiovascular system. Microscopic Functional (Physiologic) Anatomy of Skeletal Muscle fig. 10.1, p. 276. Introduction

• There are 600 skeletal muscles that have been identified on the human body.

• They are attached to bone by bundles of C.T. called tendons. These allow the muscles to pull bones closer together.


• If we examine a skeletal muscle we see that it is composed of bundles of elongated cells or fibers.

o Terminology: A Muscles cell = muscle fiber. Muscle Let's examine the structural organization of a skeletal muscle: Use figure 10.1 p 276 Muscle

• A skeletal muscle is surrounded by dense, irregular C.T. called deep fascia that strengthens and protects the muscle.

• The C.T. enclosure allows for free movement of muscle. • Between muscle fibers are collagen, elastic fibers, nerves,

and blood vessels. • The dense C.T. extends beyond the muscle at each end to

form a tendon that attaches to periosteum of a bone. o Example: calcaneal (Achilles) tendon of gastrocnemius/soleus

muscles in the calf attaches to the calcaneus bone of the foot. Muscle Fiber = Muscle Cell = Myofiber Use figure 10.1 Individual muscle fibers run longitudinally (parallel to each other) through the muscle. They number from 100s to 1000s in a muscle. Muscle fiber longitudinal section notes Fig 10.3 p 278 Note the longitudinal muscle fiber (muscle cell or myofiber) showing cross striations, nucleus, and myofibrils.

• A longitudinal muscle fiber (myofiber) is very long. o Typically 100 um (but up to 30 cm) in length, cylindrical cells,

diameter 10-100 um. • It is one of largest cells in the body.


o It is formed from many myoblasts during development, so really started out as many cells. Each cell has numerous nuclei located in the periphery, out of the way of contraction apparatus.

• Mitochondria lie in rows along the muscle contractile proteins that need ATP to drive contraction events.

Muscle cell (fiber) x-section Use figure 10.3 p278 Note the cross section of muscle fiber showing nuclei at cell periphery, sarcoplasm (muscle cell cytoplasm), myofibrils, sarcolemma (muscle cell membrane).

• Notice the nuclei are at the periphery out of the way of the contractile elements.

• Does the nucleus have a difficult time controlling such a large cell?

o No, they are multinucleate! • The plasma membrane is called the sarcolemma. Sarkos =

flesh, lemma = sheath • The cytoplasm is called sarcoplasm. • The muscle fiber (cell) is stuffed with tiny threads called

myofibrils that contain the contractile proteins. o They extend lengthwise within the muscle fiber. o They stain with alternating light and dark bands giving a striated

appearance. o These bands are called cross-striations, which give rise the

reference to striated muscle. • Myofibril = contractile elements of skeletal muscle

o They shorten to cause movement when stimulated by a neuron. o 1-2 um in diameter consisting of 3 filament types. These will be

discussed soon. Myofibril Showing Sarcomere Use figure 10.4, 10.5 p. 280.


Note the longitudinal section of a myofibril showing striations containing A band (dark), I band (light), sarcomere.

• When a myofibril is stained, you can see alternating light and

dark bands which appear as striations. o Light = I band (isotropic = scatters light evenly under

microscope). o Dark band = A band (anisotropic = scatters light unevenly under

microscope). • Each myofibril is made up of a longitudinal series of

repeated units called sarcomeres. • We will soon see these are the basic functional unit for

contraction in striated muscle. Higher magnification of a myofibril showing 2 sarcomeres Use fig. 10.4 and 10.5. p 280 Note the appearance of 1 or 2 sarcomeres showing the sarcomere, Z disc (line), H zone (band), I band, and A band. This diagram shows the relaxed, uncontracted state of the sarcomere.

• A myofibril at the molecular level is made up of myofilaments = contractile proteins.

See Fig. 10.6 p281 also • There are 2 major contractile proteins:

o 1. Myosin- thick filaments 16 nm diameter. MW = 500,000. 200 molecules/ thick

filament. They are shaped similar to a golf club with a long tail with

a club like head. The tails point toward the center of the sarcomere (M

line).


o 2. Actin- thin filaments Globular protein polymerized to form ling filaments. Two of these intertwine to form the thin filament. 8 nm diameter. MW = 60,000. Anchored at the Z discs at each end of sarcomere. 2 other proteins are associated with the thin filament:

• Tropomyosin • Troponin. • They perform a regulatory role in contraction and

will be will be discussed later. • A band (dark band in middle of sarcomere)

o It is located centrally within a sarcomere. o Consists mostly of thick filaments (myosin) and portions of thin

filaments (actin) that overlap thick filaments. See the ‘zone of overlap’ fig 10.4.

o This creates a dark, dense appearance. • I band (light bands at each end of sarcomere)

o Straddles the Z disc at the end of each sarcomere, so it overlaps with the adjacent sarcomere.

o Consists of the rest of the thin filaments (actin) only. No thick filaments.

• Z disc (lines) (narrow, plate shaped region) o The Z disc passes through the center of each I band (light),

anchors the thin filaments. o It separates one sarcomere from another.

• H zone H= helles, German for clear o The narrow H zone in the center of each A band (dark) contains

thick but not thin filaments. • M line M= middle

o The M line runs through the H zone and is the attachment point of adjacent thick filaments.

Elastic filaments See figure 10.4 to demonstrate the elastic filament.


• The 3rd most common muscle protein is a non contractile filament, the elastic filament.

• It is composed of the stretchy protein called titan (connectin) (huge MW of 3 million Daltons, largest protein with > 25k amino acids).

• It anchors the thick filament to the Z disc and then invades the M line to stabilize its structure.

• The portion that extends through and is exposed in the I band is highly elastic. It can stretch up to 4x and return to resting length without harm.

• They are relaxed in the resting sarcomere. • It is responsible for the muscle’s ability to spring back into

shape after being stretched by an external force. • Plays a major role in the precise organization of the A band. • Or in other words, maintains the normal alignment of the

thick and thin filaments. Other proteins

• Myomesin forms the M line that binds thick to titan • Dystrophin is a cytoskeletal protein that links thin filaments to

the sacrolemma. o This membrane in turn attaches to the CT matrix that surrounds

muscle fibers. This helps transmit contraction tension to the tendons.

o Defective types cause muscular dystrophy. Discussed later Changes During Contraction (the sliding filament mechanism) Hanson and Huxley, mid 1950’s proposed this idea. figure 10.7, p. 282. fig 10.8 p 283 Note in fig 10.7:

1. A relaxed sarcomere showing Z disc, I band, A band, thick filament, thin filament. 2. A contracted sarcomere showing Z disc, nearly complete overlap of thick and thin filaments.


• Remember, this myofibril is only 1 in a muscle fiber so the effects are additive throughout the muscle.

• During contraction, myosin heads (fig. 10.8) attach, pivot, and therefore pull on the thin filaments (actin) causing them to slide toward the H zone (area of only myosin fibers around M line) at the center of the sarcomere.

o It is a ratcheting type of movement. o About 1-2 um of movement. This is an additive along the entire

length of the fibril. o So if you had 100K sarcomeres end to end x 2 (um)

contraction/sarcomere = 200K um in total length contraction. Convert to cm = 20 cm.

• The sarcomere shortens, but the lengths of the thick and then filaments do not change. This is the sliding idea.

• The myosin heads ultimately release the thin filament and allow the sarcomere to relax (return to resting length).

• Shortening of many sarcomeres cause the shortening of the whole muscle fiber and the entire muscle.

In a contracted sarcomere:

• The A band is unchanged in width. • The I band is reduced or absent.

o Why? The actin in the I band slid over the myosin toward the M line.

• The H zone is almost absent. So now we have no area where myosin is not cross bridged with actin.

There are more details to this mechanism that we will discuss soon. Exercise induced muscle damage (DOMS) p.279

• Extensive exercise can cause damage to muscle cells. o Electron micrographs show torn sarcolemmas, damaged

myofibrils, and disrupted Z discs.


o Increases of myoglobin (O2 binding protein in muscle tissue), and 2 enzymes (lactic acid dehydrogenase (LDH)), and creatine phosphokinase (CPK)) are seen in the blood due to muscle cell leakage.

• Muscle soreness occurs 12 to 48 hours after strenuous exercise, called delayed onset muscle soreness (DOMS) accompanied by stiffness, tenderness, and swelling.

Assignment Question Describe and illustrate the microscopic structure of skeletal muscle. Other Structural Components of Skeletal Muscle All structures mentioned so far have been located within the sarcoplasm of a muscle fiber. Other structures within the sarcoplasm include: Fig. 10.3

• Many mitochondria o Arranged in rows through out muscle fiber. o Found close to muscle proteins that use ATP. o Provides energy (ATP) for contraction using O2, and glucose

or fatty acids.

• Sarcoplasmic reticulum (SR) o Similar to smooth endoplasmic reticulum in a non muscle

cell. o It forms a network around each myofibril and functions as a

reservoir for Ca2+ ions. o Release of Ca2+ ions into the sarcoplasm through calcium

release channels triggers the thick and thin filaments to slide over one and other and contract the muscle length (more on this later).

o The Ca2+ provides the final ‘go’ signal for initiating contraction.

• T (transverse) Tubules


o Tube or tunnel-like foldings of the sarcolemma that penetrate inside the muscle fiber.

o The tubules are open to the outside of the cell and contain ECF.

o These tubules allow a chemical message for contraction (from a neuron) to penetrate the interior of the myofiber so that all myofibrils within it can contract simultaneously (more on this later).

• The SR and the T tubules participate directly in muscle excitation and lie side by side.

o The T tubules are surrounded by terminal cisterns of the SR forming a triad appearance.

o Triad = a transverse tubule with a dilated sac of SR called terminal cisterns of either side.

o There are 2 triads per sarcomere. Excitation of Skeletal Muscle p 282-284 How is the skeletal muscle stimulated to contract? Introduction

Stimulation of skeletal muscle contraction is primarily by nerve stimulation. Nerve impulses travel from one part of the body through nerve cells called neurons. The connection between 1 neuron and a 2nd neuron (or neuron to a muscle) is called a synapse.

A look closer at nerve system messages:

• Electrical in nature along the neurons, but are chemical in nature when crossing a synapse.

• Therefore, nervous system messages are initially electrical followed by chemical propagation.

Motor Neuron Messages figure 10.2 p. 277 fig 10.11 p 287

• Two neurons in sequence o Review the anatomy of a 2 neuron circuit showing with several

axon terminals, a synaptic cleft, a 2nd receiving neuron with


cell body receiving the chemical message, with extending axon and axon terminals.

• Sensory neurons take in information to the CNS.

• Motor neurons send out information away from the CNS. Fig 15.8 p 513

o The message starts in the CNS in the primary motor cortex. o The message travels down an upper motor neuron to the spinal

cord were it synapses with a lower motor neuron (or interneuron).

• Each lower motor neuron has a threadlike axon that travels from the spinal cord (or lower brain) to a group of skeletal muscles that it controls. Fig 10.14 p 291

o Each neuron branches profusely near the muscle tissue to as many as 1000 separate muscle cells (fibers).

Motor Unit p 291

• Each motor neuron and its associated muscle cells = a motor unit. Figure 10.14 p. 291.

• The number of muscle fibers controlled by a motor unit will depend on the function of the muscle. Examples:

o A power muscle such as the gluteus maximus or gastrocnemius will have a motor unit that controls many muscle fibers (about 2000).

o A finesse muscle such as the eye or larynx muscles, will have a motor unit that controls only a few muscle fibers (about 10-20 eye, 2-3 larynx).

• The average motor unit controls 150 muscle fibers. • The strength of contraction depends in part on how many

motor units are stimulated. Neuromuscular junction Fig. 10.11 p 287, 10.2 p. 277 text p 285

• A synapse is a gap between 2 structures that can only be crossed by chemical messengers.

• The chemical messengers are called neurotransmitters.


o Neurotransmitters are stored in membrane-bound vesicles of the nerve ending (axon terminal), each containing thousands of neurotransmitter molecules.

o When an impulse moves along the axon and arrives at the axon terminal, these vesicles migrate to the membrane in the gap and release their neurotransmitter into the synaptic cleft.

o The neurotransmitter then diffuses across the synapse and joins to the receptor molecules embedded in the membrane of the nerve or muscle cell where it stimulates a muscle fiber.

o Each motor end plate typically contains 30-40 million neurotransmitter receptors.

o Drugs or toxins can affect various neurotransmitters, their receptors, or reuptake mechanisms found throughout the nervous system. Examples will be discussed soon.

Diagram of Neuromuscular Junction (NMJ) This junction is where nerve endings and muscle meet. The junctions occur near the middle of each muscle fiber. This allows a stimulus to travel in all directions of the muscle fiber simultaneously. Use figure 10.12 p. 288. Note these features in a drawing of the NMJ 3 stages: 1. Axon terminal (nerve ending) with vesicles containing neurotransmitter and motor end plate, a specialized area of the sarcolemma (plasma membrane). 2. A nervous impulse causing vesicles to release neurotransmitter from the axon terminus with neurotransmitter in the synaptic cleft area, diffusing towards the motor end plate. 3. The axon terminal at rest and neurotransmitter binding to the motor end plate. Neural muscular junction notes Now we can discuss how the NMJ functions. Overview of events


1. At rest, the axon terminal is ready to release neurotransmitter when an impulse arrives. The synaptic cleft is clear of neurotransmitter.

2. When an impulse (action potential AP) arrives, the vesicles (due to Ca++ flowing thru the protein voltage gate) move to the axon terminal and release their neurotransmitter into the synaptic cleft where it diffuses towards the motor end plate located in the sarcolemma of a muscle fiber.

3. The neurotransmitter binds to the post synaptic membrane of the motor end plate. This initiates the continuation of the impulse in the 2nd cell.

Detailed Explanation of the NMJ Physiology ACh: The NMJ Neurotransmitter

• In the case of a neuromuscular junction, the neurotransmitter = acetylcholine (ACh).

• Each motor end plate typically contains 30-40 million ACh receptors. • Each molecule of acetylcholine (ACh) works to change the

permeability of the muscle membrane (sarcolemma) to certain ions located in the ECF (Na+) and ICF (K+).

Activities of the Membranes in the NMJ Fig 12.11c p 287 Membrane resting potential ++++++++++++++++ membrane fig 12.9 p 397 - - - - - - - - - - - - - - - - - 1. Certain ion concentrations exist on both sides of the

membrane. This condition makes impulse transmission possible. a. This is due primarily to:

i. K+ leaks out at 50-100x the rate of Na+ in. So, a voltage gradient is established at the membrane surface. More negative inside the membrane suface as K+ moves out to ECF. Proteins (with neg charge) and PO4- stays behind. This establishes most of the voltage across the membrane, about -90mV.


ii. The action of the sodium/potassium pump that pumps 3 Na+ out and 2 K+ in. This pump uses ATP for energy. 1. However, K+ does not leak back in as fast as Na+ leaks back

out, so a voltage gradient is established. 2. Also, 3 Na+ are pumped out to 2 K+ pumped in so this

contributes to the voltage difference. 2. Therefore, the membrane is said to be polarized = resting

potential. a. The outside being positive (+) and the inside negative (-), like a tiny

battery. b. Example: rbc = -10mV, skeletal and heart muscle = -70mV

Membrane Events That Initiate Muscle Activation 1. If enough molecules of ACh bind to receptors sites in high

enough concentration, a depolarization will take place. 2. This is an example of a graded potential where a small area of

membrane (localized at the NMJ) has deviated from the resting potential.

3. The electrical current flow of Na+ will vary in amount (amplitude) depending on the strength of the stimulus (amount of ACh release). a. The ACh receptors contain Na+ gates that open when binding occurs. b. The ACh receptor is a channel protein that passes small these

cations (Na+). 4. The depolarization spreads along the membrane in ECF and

cytosol for only a few um before it dies out. So, only good for short distance communications.

5. When rapid depolarization occurs and spreads across the muscle cell, it is called an action potential.

Spread of the Action Potential Across the Muscle Fiber Fig 12.12 p 401 1. When Na ion rushes in at the NMJ, this changes the resting

potential into an action potential that travels locally along the muscle cell sarcolemma.


2. The action potential propagates on the muscle cell surface by triggering other Na+ channels to open that causes the entire muscle cell to contract simultaneously. a. These Na+ channels open in response to depolarization in the

membrane near them. So called voltage gated channels. b. The mechanism of contraction in the muscle cell soon.

Resetting the Resting Membrane Potential 1. One problem is left to be solved: reset the membrane for the

next impulse to be received. a. We need to get ACh away from receptors sites. b. If ACh stays, we would get a continual contraction of the muscle cell =

tetanus. 2. To get rid of ACh, the cell has an enzyme called

acetylcholinesterase (AChE). a. AChE interacts with ACh and breaks it down, therefore removing the

trigger that keeps the receptor Na+ channels open. b. After the ACh is gone, the permeability of the sarcolemma returns to

normal and therefore, goes back to resting potential, a process called repolarization.

c. This process will be discussed in more detail when we discuss the nervous system.

Muscular Disorders or Diseases the Skeletal Muscle Excitation Mechanism Myasthenia gravis box, p.302

• A progressive neural muscular disorder characterized by abnormal fatigability (weakness and atrophy) of the muscles.

• Muscles are weak, and contract with little force or speed. • It is an autoimmune disorder that is caused by antibodies directed

against ACh receptors in the motor end plate. o The antibodies bind to the ACh receptors and hinder the action

of ACh. o The disease advances as more receptors are affected and the

muscles are weaker and may cease to function.


• Anticholinesterase drugs (neostigmine) help by making more ACh available in the synapse to bind to remaining functional receptors.

• Plasmapheresis can be used to remove antibodies from the blood. Paralysis

• Inability to voluntarily control skeletal muscle. A general term. • Usually due to nerve damage (denervation - severed nerves), as

muscle will still respond to direct (external) stimulation. • However, the lesion could be of nerve or muscle origin.

Fatigue p.290

• If muscle is over stimulated the strength of contractions becomes progressively weaker to the point where they won't respond.

• The muscle is in a state of continuous of contraction. o Example: writers cramp, a temporary contracture.

• It occurs when the muscle cannot release adequate Ca++ from the SR .

• Surprisingly, ATP levels are similar to resting muscle. • Factors that cause this are:

o Insufficient O2, depletion of CP, depletion of glycogen, build up of lactic acid and ADP, or ionic imbalance (too much Na+ inside, too much K+ outside), too little ACh in synapse in response to stimuli (APs).

• So, powerful muscle efforts reach this state quickly, while lighter effort endurance activities can last for hours in a person who exercises regularly.

o The question becomes, can the mitochondria keep up with the level of muscle activity?

Muscular Dystrophies box, p.302

• Inherited muscle destroying disease, where muscle cells degenerate and may be replaced with fibrous C.T. or fat.


o Wheel chair use may be the result at teen years, followed by death at 20-30.

• Most common is Duchenne M.D., a sex-linked disease of boys, diagnosed usually from ages 3-5.

o Females are the carriers and transmit the disease to their sons (1 in 3500 births).

o X chromosome linked; boys only have one X so recessive gene is expressed in a single dose.

o A protein in the sarcolemma, dystrophin, is missing and seems to lead to muscle fiber degeneration.

• No treatment is currently available, however gene therapy (myoblast transfer and plasmid injection) is being investigated.

Drug Effects on Muscular Excitation Cholinesterase Inhibitors

• Cholinesterase inhibitors bind to AChE and prevent degrading ACh. o Examples: o DFP (a standard organophosphate, diisopropyl-

fluorophosphate) o parathion (both nerve pesticides) o sarin nerve gas o neostigmine (chemical drug used in treating myasthenia

gravis). • The inhibition of AChE causes spastic paralysis of the muscles, a

state of continual contraction. o There is an immediate danger of suffocation if laryngeal and

respiratory muscles are affected. o The poisoned person should remain still and quiet to avoid a

startle response that could escalate into dangerous muscle spasms.

• Atropine, an ACh antagonist, is given as an antidote treatment for cholinesterase inhibitors.

o Atropine blocks ACh at post ganglionic cholinergic musarinic receptors.

o These receptors affect smooth muscle in GI, pulmonary, exocrine, heart, eye.


o Used in eye exams to dilate the pupils Curare

• Causes flaccid paralysis by binding to ACh receptors without causing stimulation, and blocking ACh action.

• Therefore it blocks the neuromuscular junction. • Respiratory failure can result. • Used by South America Indians to poison arrows. • Historically used to relax muscles in abdominal surgery (abdominal

and diaphragm muscles) so they can be moved aside. o Now replaced by newer drugs.

Blackwidow spider venom

• Contains many toxins of which one promotes constant release of neurotransmitter.

• Results in tetanus, a state of constant contraction. • When the diaphragm muscle is affected, breathing action is ceased.

Botulism

• In botulism, a toxin called botulinum is produced by the bacteria, Clostridium botulinum. It is ingested with contaminated food.

o This toxin prevents the release of synaptic vesicles containing ACh, and therefore blocks nerve transmission.

o A type of flaccid paralysis results. o It is the most potent toxin known: 0.0001 mg will kill a person.

1/2 lb. could kill all humans. Assign question What is a motor unit? How does it related to total strength of contraction? What is a neuromuscular junction? What events occur at the junction?


The Sliding Filament Theory (1954, Hanson and Huxely) Overview P 282-6

• These 2 investigators proposed that skeletal muscle shortens during contraction because the thin (actin) filaments slide over the thick (myosin) filaments.

o Then, they would overlap to a greater degree. • Rather than:

o The previous idea that the filaments change in length themselves, or possibly fold.

Fig. 10.7 p.282 • In a relaxed muscle the thick and thin filaments overlap

slightly, but during contraction, the thin filaments penetrate more and more deeply into the central region of the A band.

o The thin filaments pull the Z disc they are attached to toward the thick filaments which shortens the sarcomere.

o Remember, the I band and the H zones disappear as the thin filaments move to the center. The A band stays the same length.

o Only the length of the sarcomere changes, not the length of the filaments!

• This shortens the whole muscle fiber and ultimately the whole muscle.

• Their model is known as the sliding filament mechanism of muscle contraction.

Closer Look at the Events During Contraction Now take a look at contraction in a step-by-step fashion. 17 steps will be described during a muscle contraction event. Note: Figure 10.12, p. 288, explains these events in 9 steps. It is not important that you can name a step, but that you can explain how muscle contraction works.


1. Nerve impulse arrives at neural muscular junction from the CNS. (The sarcolemma is at a resting potential at this point). Fig 10.12,1

2. ACh (acetylcholine) release from axon terminals. Fig 10.10,2 3. ACh binds to active sites (protein receptors) on motor end

plate. Fig 10.12,2 4. Development of a graded potential that triggers a muscle action

potential (AP). Fig 10.12 2,3 a. ACh receptor protein channel increases permeability of Na+

into sarcoplasm. i. A graded potential develops as the chemically gated

receptor/channel opens in response to ACh binding. ii. This is a localized (a few um), small deviation from the

resting membrane potential. b. Acetylcholinesterase (AChE) begins to degrade ACh in the

synaptic cleft. c. If there is enough ACh action to open enough Na+ channels

(that is, enough of a graded potential), an action potential (AP) will occur.

(Steps 1-4 represent nerve impulse recognition due to a local, graded potential at the neuromuscular junction.) 5. Na+ enters muscle fiber, depolarization of sarcolemma occurs

= action potential. a. Voltage changes to a less negative charge across the

sarcolemma. b. Voltage gated Na+ channels open in response to the

original chemical gated Na+ channels opening. 6. The action potential spreads away from the end plate in all

directions on the sarcolemma as more voltage gates are triggered and ultimately descends into the T (transverse) tubules where depolarization continues.

7. When the action potential continues down the T tubules that penetrate the sarcoplasm, it stimulates voltage sensing receptor membrane proteins that link with the sarcoplasmic reticulum (SR) membrane channels for Ca++ release.


(Steps 5-7 represent depolarization. Fig 10.12, 4) 8. The SR responds (within 1 ms) to the action potential by

opening Ca+2 release channels which floods the surrounding sarcoplasm located between the thick and thin filaments. a. Ca+2 flood last about 30ms. b. A continuously active ATP-dependent pump is pumping

Ca+2 back into the SR. 9. Ca+2 combines with the regulatory protein troponin that is

bound to tropomyosin. a. Tropomyosin is wound around the actin filaments, blocking

the binding site on actin for myosin when Ca+2 levels are low.

10. Troponin changes shape, which moves the troponin-tropomyosin complex deeper into the actin helix structure, and exposes the myosin binding sites on actin.

See figure 10.9, p. 284, diagram of myosin with heads. 11. Myosin heads can now attach (cross bridge formation) to actin

binding sites on thin filament. Figure 10.8, 2, p. 283, actin myofilaments and myosin filament with heads attaching to actin binding sites. 12. Myosin head flexes toward the center of the sarcomere,

pulling actin filaments of sarcomere toward each other (toward the middle of the sarcomere). a. This is called the ‘power stroke’ of contraction. Fig. 10.8 3,4, p. 283, myosin with head in the cocked forward position and then flexing back onto the myosin filament.

13. Once the myosin head is flexed, ADP is released from the head and its ATP binding site is exposed.

14. The myosin head detaches from actin binding site under the influence of ATP binding. Fig 10.8 4 a. This is called ‘cross bridge detachment’. b. The myosin head has an ATPase activity in the ATP binding

site. c. ATP is split and transfers energy, ADP, and P group to the

head.


d. Energy from ATP returns the myosin head to the cocked forward position.

e. The myosin head is now in its upright, high energy position, back to where it started.

f. You can now see that the myosin is ‘precharged’ so when an AP is received, it is ready. This state can be achieved as long as ATP is available.

g. APs received now will cause the myosin to reattach and further pull the actin along.

h. This gives the impression of myosin heads ‘walking’ over the adjacent actin filaments during muscle shortening.

(Steps 11-14 are repeated during a contraction event if ATP and Ca+2 are available.) Rigor mortis box, p. 285

• Notice that ATP is responsible for myosin heads detaching from actin, which leads to muscle relaxation. In other words, myosin cannot detach without ATP present.

• This is illustrated by rigor mortis. o When a person dies, no more ATP is synthesized as no more

02 and glucose are supplied to the tissues. o The myosin heads cannot detach themselves from actin

resulting in a condition in which muscles are in a state of rigidity (they cannot contract or stretch) called rigor mortis.

o This state lasts about 24 hours and disappears as the tissues undergo autolysis. (Lysosomes are broken down and release their contents.)

15. Ca+2 is returned to the SR by the Ca+2 active transport pump

(requires ATP) and the Ca2+ channels close. a. Sarcoplasm is now Ca+2 poor. b. (The Ca+2 is bound to a protein, calsequestrin, in the SR. If

this high concentration of Ca+2 is not bound it would combine


with PO4- to form hydroxyapatite, as in bone, which would kill

the cell.) 16. Troponin again covers actin binding sites. Therefore no

myosin-actin interaction can occur. 17. Muscle fiber relaxes. Movement of relaxation is due to:

a. "Elastic effect" of coiled elastic fiber (titan) molecules, and/or: b. Due to pull of C.T. within muscle.

ATP and Contraction ATP is required for 3 major roles in contraction:

1. Reposition (cocking) of myosin molecule when muscle is relaxed. Fig 10.8, 1

a. This reaction transfers energy from ATP to the myosin head even before contraction begins.

b. The myosin heads are in an activated state (cocked and energized).

2. Detachment of myosin heads from actin once the power stroke is complete. Fig 10.8, 4

a. Myosin remains flexed and bound to actin until another ATP molecule binds it. This is the recovery stroke.

b. Each cycle of the head consumes one molecule of ATP. (Some evidence disputes this.)

3. Powers the Ca+2 active transport pumps that rapidly remove Ca+2 from the sarcoplasm back into the sarcoplasmic reticulum. Fig 10.12, 7

a. The concentration of Ca+2 is 10,000 times lower in the sarcoplasm of a relaxed muscle fiber than inside the SR.

Muscle stores enough ATP for 4-6 seconds of activity. It is regenerated in 3 ways: Fig. 10.13, p.2289 text p 289-90


1. Interaction of ADP with creatine phosphate (CP). (Phosphagen system)

a. CP is an energy rich small molecule only found in muscle cells, at 3-5x amount of ATP. Fig 10.13 a

b. When ATP levels drop during work, CP is used to make ATP quickly.

c. Duration of benefit: ATP + CP will provide muscle power for about 15 seconds.

i. What can you do in 15 seconds? Run away! Good for a 100m dash! Climb a tree! Attack!

d. Creatine is a popular dietary supplement to enhance muscle mass among power athletes.

e. Products of reaction: 1 ATP, 1 CP, 1 creatine. CP is built back up during rest periods.

2. Stored glycogen via the anaerobic glycolysis pathway. (Glycogen-Lactic Acid System) fig 10.13 b

a. When activity level surpasses the O2 level available for the mitochondria to use for respiration, this system takes over.

b. Products: 2 ATP per glucose, lactic acid. c. No oxygen is needed! Called an anaerobic process. Lactic acid

can be used by liver cells, heart muscle, and kidney cells to make ATP.

d. However, in skeletal muscle, build up of lactic acid lowers pH and causes pain.

e. Duration of benefit: 30-40 seconds of maximal activity. Example: 300m race

3. Aerobic respiration. Fig 10.13c a. Occurs in mitochondria that are in great numbers in

muscle. b. The process is slower than glycolysis but yields much

more ATP but requires oxygen. c. Can burn glycogen (glucose), fatty acids, or protein. d. Products: 36 ATP per glucose. CO2, H2O given off as

waste. Heat. e. Duration of benefit: after 30 seconds to hours. Note: to

burn fat, use light to moderate exercise so mitochondria can keep up with energy needs.


Oxygen Consumption after Exercise p 291 Oxygen debt (older term) = recovery oxygen uptake (newer term)

• The amount of oxygen that must be ‘paid back’ to the body following exercise.

• You know you breather harder, more vigorously after exercise to take in more O2 and remove CO2. While the body is hotter than normal and the heart and breathing muscles are working hard, more oxygen is needed.

o Example: when get out of class early and run to car! • A 100m dash requires about 6L of O2 for totally aerobic respiration,

however you can only take in about 1.2 L (VO2 max). o VO2 max is the maximal rate of oxygen consumption by aerobic

respiration. This is largely genetically determined but can be increased 20% or so by training. Elite athletes have double this rate.

• So, you develop an O2 debt. Extra oxygen received during recovery does 3 things:

1. Convert the lactic acid back into glycogen via the liver. 2. Resynthesize creatine phosphate and ATP 3. Replace oxygen removed from myoglobin in the muscle during

exercise. Physiological Properties of Muscles

• Stimulus = an impulse. • An impulse may travel along a motor neuron that is not

strong enough to cause a contraction. Fig 12.11 p 399 • Study the graph of electrical potential in millivolts (mV) vs.

time at the membrane surface. o It should show a range of -70 mV to +40 mV on y axis. o A stimulus that does not cause a response by the muscle is

called subliminal or subthreshold stimulus.


o By increasing the stimulus, a barely perceptible response may be obtained = liminal or threshold response.

o It is just strong enough to cause a depolarization and production of an action potential. Action potentials trigger contraction.

o This is a change from –70mV to –55mV at the membrane surface.

o A maximal response is one in which all the fibers of the muscle are active.

Assign questions What is the sliding filament mechanism? Describe the role of calcium and regulator proteins in the sliding of filaments. What changes permit a muscle fiber to relax after contraction? Grading of Strength of a Contraction or How can we control how much strength a muscle produces?

• An individual motor unit fires all muscle fibers in that unit in an ‘all or none’ fashion.

• All fibers contract to there fullest extent. The whole muscle tension however can be adjusted. There are 2 ways to control strength of a contraction:

1. Recruitment of motor units. 2. Altering the contractility of individual muscle fibers.

1. Recruitment of motor units. (multiple motor unit summation) p. 292

An individual neuron branches to many different muscle fibers. The neuron and the muscle fibers it activates are together called = motor unit. a. Motor units vary in size b. A small motor unit may consist of as few as 10 fibers, while a large

one may consist of several 100. i. Example: Fingers contain very small motor units so they can carry


out fine movement. c. Simply speaking: If a muscle needs more force, it will recruit (activate)

more motor units. If not so much force is necessary, less are recruited.

d. The strength of the electrical stimulus determines the amount of motor units recruited. i. Threshold stimulus causes the first observable muscle contraction.

1. A threshold stimulus recruits the most excitable motor neurons first that control the smallest motor units.

2. Example: the hand is used to lightly pat a cheek ii. Maximal stimulus is the strongest stimulus that still causes

increased contraction. 1. A maximal stimulus recruits the strongest contraction possible

by recruiting the larger motor units driven by less excitable neurons.

2. Example: a sharp slap to the face iii. The primary function of motor unit recruitment is create smooth

movements not just more contractile force. 1. We demonstrated this in lab the first night with the stimulator, a

transition from jerky contraction to a smooth maximal contraction.

2. Experience is important in knowing how many motor units to recruit. a. Other wise you could hurt yourself or damage something. b. Example: I

i. If you pick up a milk carton that you thought was full and is empty you will probably spill some milk.

ii. So, when you pick something up that you think is heavy but is an illusion, you will recruit too many motor units and the muscle will over react.

iii. Can you think of examples where you have done this? iv. A young child with a small pet?

3. Motor units usually contract asynchronously in that some motor units are in tetany and some are relaxed. This prevents or delays fatigue.

2. Altering the contractility of individual muscle fibers. This means changing the properties of muscle fibers irrespective


of how many fibers are involved. There are 2 ways to change the contractility of fibers. 1. Increase the frequency of stimulation to individual fibers. 2. Vary the length of the fiber (length-tension relationships). 1. Increasing frequency of stimulation.

• First, let’s see how we can hook a muscle up to the following apparatus and measure changes in force:

o Draw a frog muscle anchored at one end, and anchored to a force tension transducer at the other end. Show the transducer wired to a physiograph that has a paper recorder.

o Keeping the muscle at a fixed length and stimulating it, we can measure a change in tension overtime:

• A single muscle twitch Figure 10.15 p. 292. o Draw a myogram showing a single isometric twitch, with tension

on the Y axis and time on the X axis. o The tension produced from the stimulation is called a twitch,

because it takes place when the muscle length is fixed. o It is called an isometric twitch = tension but no shortening. o As opposed to isotonic twitch = tension and shortening.

• Summation effect or wave summation of 2 or 3 stimuli o If 1 stimulation quickly by another, you see what is called the

summation effect or wave summation = the tension produced in the second stimulation will be added to the first, that is it will be stronger. Figure 10.16b page 293. See the myogram with tension on the Y axis and time on

the X axis. The first stimulation, S1 is to the right followed by the second stimulation, S2 near the peak of the first contraction.

o This occurs because the cell membrane has repolarized (takes about 5 ms) but the muscle sarcomeres have not completely relaxed (are partially contracted because it takes time to pump Ca+2 back into SR) (takes 10 –100 ms) and more calcium is released that adds to some of that released in the first stimulus.


However, summation is not an infinite effect which leads us to tetanus.

• Complete (fused) and incomplete (unfused) tetanus o If there is repeated stimulation, tension will reach a certain

plateau and stay there (this is known as tetanus). o Neurons normally deliver nerve impulses in volleys, not single

impulses as we demonstrate in class. o This is how we have smooth and sustained muscle activity.

Figure 10.16d, p. 293. See the myogram demonstrating complete (repeated fast

stimulations, 80-100/sec) and incomplete tetanus (repeated slow stimulations, 20-30/ sec).

• Incomplete (unfused) tetanus fig 10.16c • Muscle can only partially relax between stimuli. • Occurs at 20-30 stimuli/sec. • Complete (fused) tetanus

o Muscle has a sustained, smooth contraction with no relaxation. o Occurs at 80-100 stimuli/sec. o This is how muscle stimulation usually occurs with volleys of

stimuli in rapid succession from the neurons (CNS). o The tension (strength) is 2-4 times the tension of a single

twitch. o Eventually, the muscle will run out of ATP and will fatigue (force

will go to zero). Another way to alter the contractility of a fiber: 2. Vary the length of the fiber (length-tension relationship)

• % Sarcomere length vs. tension p285 o If we examined this at the magnification level of the myofibril,

we could plot sarcomere length vs. tension. Figure 10.10. p.285 o Draw a myogram with tension on the Y axis and sarcomere

length in um on x axis from short to long. o Maximum tension occurs at about 2.2 um. o This is the ‘sweet spot’ for fiber overlap and strength.

• What is the reason for this? Let's look at a sarcomere at the different lengths.


o View the sarcomere at 2.1 um and at 3.8 um length. Figure 10.10. See that the more contracted the sarcomere, the greater

the overlap between thick and thin filaments. The more they overlap, the more cross bridges which can

connect and hence, more tension can be produced. But thick filaments crumple as they are compressed by

the Z discs when sarcomere shortening is extreme. The thick and thin filaments interfere with each other and

break myosin bonds. o If the sarcomere is stretched so that the thick and thin filaments

cannot overlap very much, contraction decreases. o If stretched to about 175% of optimal length, no myosin heads

can crosslink with thin filaments, and no contraction can occur. o In the body, resting muscle fiber length is maintained at 70-

130% of the optimum, because of the way muscles are anchored to bones and C.T.

Types Of Skeletal Muscle Contractions Fig. 10.17 p294 Isotonic Contractions: the contraction of movement

• Tension is produced and overall shortening of the muscle occurs as a load is moved through the range of motion to the joint .

• Example: These contractions draw two bones together and serve to bring about movement.

o (concentric contraction: muscle shortens during contraction fig 10.17a

o (eccentric contraction: muscle lengthens during contraction fig 10.17b

o These 2 types together bring about coordinated, smooth movements.

Isometric Contractions: the contraction of stabilization. Fig 10.17c

• Tension is produced but no shortening of the muscle occurs. • Energy is still used! Crosslinking occurs but no sliding of filaments.

o Example: These contractions serve to keep the body fixed in position as in maintaining posture. As in the neck, trunk, legs, feet.

• Most body activities involve both isotonic and isometric contractions.


Twitch A single isotonic response as a result of a brief threshold (liminal) stimulus.

• (This is not the type of twitch you feel in your body due to being tired or a chemical imbalance).

• The muscle contracts quickly and then relaxes. • A twitch can be demonstrated by an instrument that produces a

myogram, a tracing of a muscle contraction. A simple muscle twitch consists of 3 phases, they are: Fig. 10.15, p.292 1. 1.Latent Period

a. The time from stimulation of the muscle until shortening of the muscle begins. The latent period is a “lag time”.

b. Duration = about 2 ms. c. During this period of time the following events of muscle contraction

are occurring: i. Depolarization, action potential triggered (1-2 ms), repolarization

begins. ii. Diffusion of Ca+2 iii. Establishment of actin/myosin bonding

d. Uptake of elastic connective tissue in muscle to bone connection. 2. Contraction Phase

a. Tension and shortening of the muscle occurs. b. The upward tracing represents this phase. c. Repolarization is completed and refractory (non excitable) period ends

(within 5 ms). d. Duration = 10-100 ms.

3. Relaxation Phase a. Muscle goes back to it resting state. b. The downward tracing represents this phase. c. The Ca+2 is actively transported back into the SR which results in

relaxation. d. The sarcomere begins to recoil back to resting length. e. Duration = 10-100 ms.


Types of Muscle Skeletal Muscle Fibers table 10.2 p.296 In humans we see 3 types of skeletal muscle fibers classified on 2 factors: 1. How fast the muscle will twitch, and 2. Method of ATP generation. 1. How fast a muscle will twitch (due to how fast myosin head ATPase

splits ATP). Factors: a. How much myoglobin is in the muscle fiber.

i. Myoglobin is a respiratory pigment that binds O2 for ATP generation.

ii. It makes muscle appear red. iii. If absent, then fiber appears white.

b. Number of mitochondria available i. The more available, the more sustained level of activity. ii. Number of capillaries that serve the muscle fiber. iii. The more capillaries available, the more nutrients and wastes can

be transported. 2. Metabolic way used to generate ATP. Review fig. 10.13

a. Respiration uses O2 and occurs in the mitochondria = oxidative metabolism.

b. Fermentation occurs when O2 is not available = anaerobic metabolism.


Table of Characteristics of Skeletal Muscle Types Postural Walking Quick Power Moves Structural Features Slow Oxidative SO Fast Oxidative FOG Fast Glycolytic FG Diameter or Fiber Smallest Intermediate Largest Color/Myoglobin Red/large Red-pink/large White/small Mitochondria Many Many Few Functional Features Slow Oxidative Fast Oxidative Fast Glycolytic ATP Production Aerobic (O2) Aerobic (O2) Anaerobic glycolysis ATP use/Veloc. of Contrac. Slow Fast Fast Resists Fatigue High Intermediate Low Glycogen Stores Low Intermediate High Order of recruitment 1st 2nd 3rd Activities/Function/Location: Slow Oxidative SO:

• Slow twitch, type I, fatigue resistant fibers • Maintain posture (anti-gravity muscles), endurance running. • Location: Back and neck muscles.

Fast Oxidative FOG:

• Fast twitch A, type IIA, fatigue resistant fibers • Walking, sprinting. • Location: Leg muscles.

Fast Glycolytic FG:

• Fast twitch B, type IIB, fatigable fibers • Rapid, intense movements of short duration. Ball throwing, weight

lifting. • Location: Arm muscles.

Other animals use of muscle cell types Concentrations of fast and slow twitch muscles can be observed in other animals as well as humans.

• The light and dark meat of a chicken has to do with concentrations of different types of muscle fibers.

o A chicken uses it’s breast muscle (white meat) for short flight if at all = fast twitch. The legs (dark meat) of a chicken serve for endurance = (slow twitch).


o What type of meat would you expect to find in the breast of a migratory duck? Dark meat = slow twitch for endurance.

Implications of fast twitch and slow twitch muscles in sports:

• The proportion of slow twitch versus fast twitch muscles you possess is genetically determined and cannot be changed dramatically.

• In other words training and conditioning can do some change. Endurance training can change FG fibers to FOG fibers. Power lifting will increase size and strength of FG due to increase in fiber size and strength.

o Example: o Alberto Salazar (marathon runner): 92% red slow twitch, 8%

white fast twitch. • Sprinters contain about 60% fast oxidative. • Weight lifters have about equal amounts fast glycolytic and slow

oxidative • Determination of muscle fiber ratios can be done by muscle biopsy.

See transverse sec., p.296. Anabolic Steroid abuse

• Testosterone (found in men) and growth hormone influence muscle growth.

• Anabolic steroid drugs are testosterone like and are abused by athletes to increase strength and endurance.

o Problems: liver cancer, kidney cancer, heart disease, aggressive behavior, mood swings. Females: sterility, facial hair, deep voice, atrophy of

breast and uterus, menstrual irregularities. Males: testes atrophy, less sperm production, baldness.

Frequency of Stimulation

• Tetanus o The sustained contraction of a muscle due to increased

frequency of stimulation. o The result of summation of twitches. Fig. 10.16d p.293 o Tetany results from the summation of twitches and the amount

of force generated is 2-4 times the force of a single twitch.


o When the frequency of the stimulation is such that there is no hint of reduced tension or force between stimuli, it is called complete tetany or fused tetany. 80-100 stim/sec

o When the frequency of stimulation is reduced slightly, you can see partial muscle relaxation occurring between contractions, this is called incomplete tetany or unfused tetany. 20-30 stim/sec

o Incomplete tetany can result in trembling (shaky) movements of the limbs observed in some individuals.

o Normal muscle contractions with smooth movement are a result of complete tetanic contractions.

Treppe (no longer in Tortora) Is the increased strength of contraction as a muscle ‘warms up’ due to identical stimuli too far apart for wave summation to occur. It is also known as the ‘staircase effect’, as the muscle steps up its strength with each contraction. Draw diagram of treppe with identical stimuli too far apart for summation. (No diagram in Tortora) Treppe can be explained as follows: 1. A progressive buildup of Ca2+ in the sarcoplasm probably accumulates

because the stimuli release Ca2+ faster than the Ca2+ pump can move them back in to the SR. a. The troponin becomes saturated for maximum binding to myosin

heads. b. Eventually the inflow and outflow of calcium ions equalize and the

strength of contraction will level off 2. In your warming muscles, the sarcoplasm becomes also becomes less

viscous with more heat and the internal resistance of the muscle is lessened allowing more energy to be directed to muscle shortening and less to overcome resistance. a. With increased heat, the enzyme systems become more efficient. b. This is the basis for the warm-up period for athletes.

Muscle Tone p.293


• Tone is a sustained partial state of contraction in the muscle. • They are involuntary spinal reflexes responses to activation of stretch

receptors in muscles and tendons. • Movements are not produced. • Tone is maintained in the body without fatigue by the alternation of

different motor units. It serves to keep the body in a state of readiness for activity at all times.

Hypotonia see box p.302

• Refers to decreased or lost muscle tone, resulting in flaccid (flattened) shape.

Atrophy see p.279

• Wasting of muscle tissue where muscle fibers decrease in size as myofibrils are lost.

Hypertrophy see p.279

• Opposite of atrophy. • Refers to an increase in diameter of muscle fibers where myofibrils,

mitochondria, and SR are increased. Capillaries servicing muscle fibers are increased too. No increase in # of cells.

• Due to forceful, repetitive strength training, which results in increased capacity for forceful contractions.

Muscle tone can be lost quickly. See p.279.

• If muscle usage is prevented by a cast (disuse atrophy), or by a severing of the nerves (denervation atrophy), the muscle fibers begin to atrophy in just a few days.

• Muscle ¼ size in 6 – 48 mos. of disuse. • Prolonged inactivity can lead to degeneration of the muscle fibers and

they may be replaced by C.T., including fat, which cannot be reversed when complete.

• Direct stimulation of the inactive muscle using a muscle stimulator may prevent atrophy until the muscle is removed from the cast or the severed nerve fibers can remake connections.

• The important thing to realize is that muscle health is maintained in part by utilization - “use it, or lose it!”


Smooth Muscle table 10.2, 300 Introduction

• Smooth muscle is also called involuntary muscle (under ANS control) and nonstriated muscle (lacks organized sarcomeres).

o Actin and myosin myofilaments are present but are not regularly arranged leading to the absence of light and dark bands that cause the striations in skeletal muscle tissue. Fig10.19

• Smooth muscle cells have a sarcolemma but contain fewer myofibrils than skeletal muscle.

• Contractions start slowly and last a relatively long time. • Maintains steady pressure in GI tract and blood vessels.

Characteristics of smooth muscle in comparison to skeletal muscle table 10.2 Smooth muscle has: 1. 7 times less actin & myosin in smooth muscle than skeletal muscle with

no sarcomeres. 2. Lower levels of ATP (& creatinine phosphate) 3. Fewer number of mitochondria with slow contractions. 4. Smooth muscle cells lack T-tubules. Slower onset of contraction. 5. Have poorly developed sarcoplasmic reticulum. Takes Ca2+ longer to

diffuse. Some Ca2+ leaks in from ECF. Also delays in sequestering Ca2+ for longer contraction.

6. Contraction regulated by not only neurotransmitters (ACh, NE by ANS), but also by: hormones, local chemical changes (pH, O2, CO2), and stretching.

So smooth muscle is designed for slow reacting, but prolonged contractions. Note: The two types of smooth muscle will not be discussed.


Abnormal Contractions Of Muscle Tissue Spasm p 302

• A sudden involuntary muscle twitch (contraction of short duration), usually due to a chemical imbalance.

Cramp p 302

• A sustained, painful, spasmodic (tetanic) contraction of a muscle. • Can last more minutes to hours. • Severe cramps usually occur when the muscle is shortened (when

there is little pull on the tendons). • Usually occurs at night or after exercise. • May reflect low blood sugar, electrolyte depletion (Na+ or Ca+2), or

dehydration. Sensory impulses then trigger a reflex in the spinal cord neurons to initiate contraction.

• It is not known what actually happens at the level of a sarcomere during a cramp. However, the pull on the tendons of muscles are constantly monitored by sense organs called golgi tendon organs. p. 506 fig 15.4

o Golgi tendon organs act to inhibit or “apply the brakes” to muscular contraction to prevent the development of too great of tensile force that could result in injury to the muscle or tendon.

o Learning how to keep the golgi tendon organs from working may be an important part of strength training.

o Maximal vigorous contractions when the muscle is in a shortened position seems to increase the probability of cramping.

• How can you relieve cramps in light of this information? o Simply forcing the muscle into its longest position (stretching)

will create tension on the golgi tendon organ. o The inhibition caused by the golgi tendon organ will then stop

the cramp. Convulsions

• Violent, involuntary contractions of whole groups of muscles. • Convulsions occur when motor neurons are stimulated by factors

such as fever, poisons, hysteria, and changes in body chemistry due to drug withdrawals.


• The stimulated neurons send seemingly senseless impulses to the muscle fibers.

• This is a nervous disorder not a muscular disorder. Fibrillation p 302

• Uncoordinated contraction of individual muscle fibers so that the muscle fails to contract smoothly.

• Cardiac muscle is most prone to this type of activity and is recorded by electromyography.

Assign question What is a myogram? Describe the latent period, contraction period, and relaxation period of a muscle twitch contraction. Distinguish between tetanus incomplete, complete tetanus, and the staircase effect. Contrast the structure and function of slow oxidative, fast oxidative, and fast glycolytic skeletal muscle.


Introduction To The Nervous System Chapter 12 p386 fig 12.1 The nervous system in conjunction with the endocrine system is responsible for coordination of all of the other human body systems. The nervous system is a ‘wired’ system with discrete pathways and local actions. The effects of nervous stimulation are usually immediate and short lived.

Example: muscle movement The endocrine system is specialized to control activities that require duration not speed. Hormones are secreted into the bloodstream and have wide ranging effects on target cells that contain hormone receptors.

Examples: growth patterns, reproduction cycles, metabolism (glucose), water balance

Functions of the Nervous System: Fig 12.2 p 388

1. Sensory: afferent neurons

a. Millions of sensory (efferent) receptors monitor changes both inside and outside the body.

b. The changes are called stimuli and the information gathered sensory input.

i. Examples: Internal: stretching of stomach, pH changes in blood.

ii. External: Smells, sights, sounds, pressure, pain. 2. Integration: interneurons

a. It analyzes sensory inputs, stores some information, and makes decisions about what should be done each moment.

3. Motor: efferent neurons a. It may cause a response by activating effector organs: muscles

to contract and glands to secrete. b. This response would be called motor output.

4. Conceptual thought


a. Capacity to record, store, and relate information received and use it at a later date.

b. A high level of self awareness. c. The human brain represents the peak of development of animal

brains. d. This trend has enabled such adaptive capacities as learning,

introspection, planning, speech and language. e. Indeed a single humans art, speech and ideas, and deeds may

affect literally millions of other humans, and maybe the biosphere itself.

Classification of the Nervous System It is very important that you understand which divisions of the nervous system are anatomical structures (i.e. a structure you would actually see during the course of a dissection or operation) and which nervous system terms are based on function that is, how it works. The next 2 diagrams are in your course outline. Anatomical Classification of the Nervous system Fig. 12.1, p387 Nervous System Central Nervous System Peripheral Nervous System 1. Brain 1. Nerves 2. Spinal Cord 2. Ganglia 3. Sensory Receptors From an anatomical perspective the nervous system has 2 major divisions: 1. The Central Nervous System. 2. The Peripheral Nervous System.


The Central Nervous system consists of the brain and the spinal cord and nothing else! Any other nervous system structure that connects to the brain or spinal cord would be a part of the Peripheral nervous system. The 3 major components of the peripheral nervous system are: 1. Nerves 2. Ganglia 3. Sensory receptors 1. Nerves fig 13.10 p. 434

a. Simply defined a nerve is a bundle of neurons or nerve cells. b. They can be motor, sensory or mixed. c. 2 important categories of nerves that are a part of the peripheral

nervous system: i. Cranial nerves (12 pr.) that branch to and from the brain.

1. You need to know these for exam 2. See the detail in the course outline.

2. For each nerve, know number, name, functions: sensory or motor or both. These are discussed in table 14.3 p. 485-489 of chapter 14.

ii. Spinal nerves (31 pr.) that exit the spinal cord bilaterally from between each vertebrae. Fig 13.2 p 422 Discussed on 433-435 fig 13.11.

2. Ganglia fig 13.3 p424 a. Ganglia are aggregations of nerve cell bodies. Ex. Dorsal root

ganglia. 3. Sensory receptors fig 15.1 p500

a. Sensory receptors or sense organs as they are sometimes called serve to give the body information about the immediate environment, both internal and external.

b. They include the special sense organs involved in your sense of taste, touch, sight, hearing, or smell.

Functional Classification of the Nervous System Fig 12.2 p388 Note: we will not discuss the Enteric Motor Neurons(ENS) classification.


Nervous System Afferent (Sensory) Efferent (Motor) Autonomic Somatic

CNS integration

Sympathetic (Stress) Parasympathetic (Calm) Afferent Division

• The Afferent division of the nervous system is responsible for carrying information toward the brain.

• The afferent division is also called the Sensory division as it picks up information about the environment and takes that information to the brain (CNS).

Efferent Division

• The Efferent division of the nervous system is responsible for carrying information out and away from the brain.

• The Efferent division is also called the motor division. We will consider in this class the Enteric Nervous System (ENS) to be part of the Autonomic nervous system (ANS)

The Efferent division is further divided into 2 parts based on whether the information coming from the brain is under voluntary or involuntary control. 1. Somatic Nervous System

• The somatic portion of the efferent division is under voluntary control and is composed of somatic motor nerve fibers.

• It is the part of the nervous system that serves to innervate skeletal muscle tissue.

• We have already discussed how you have voluntary control over skeletal muscle actions.

2. Autonomic Nervous System (ANS) fig 17.1 p567 p 566-581


• You do not have control over the information that passes through the ANS. For that reason the Autonomic nervous system is sometimes referred to as the automatic or involuntary division.

• The specific tissues that are innervated by visceral motor nerves of the autonomic nervous system are:

o Smooth muscle, cardiac muscle, and glands. Let’s discuss the 2 divisions of the ANS: a. The Sympathetic division. b. The Parasympathetic division. Parasympathetic Division

• The parasympathetic division attempts to conserve body resources. Restore after exertion.

• It is primarily dominant under calm conditions- ‘rest and digest’. • SLUDD= salivation, lacrimation, urination, digestion, defecation. The

3 Decreases: heart rate, diameter of airway, diameter of pupils. Sympathetic Division

• The sympathetic division dominates under conditions of stress. • It serves to prepare for the quick utilization of body resources. • The sympathetic division is said to be the division that prepares you

for “fight or flight”. o Supports vigorous physical activity and ATP production. o E situations: exercise, excitement, emergency, embarrassment.

Aided by hormone (E and NE) release from adrenal medulla. • Dilates eyes, increases heart rate and contractions, increase BP,

dilate airway, increase blood to skeletal and cardiac muscle, liver, fat tissue, glycogenolysis, lipolysis, digestion inhibited. Table 17.4 p 580-1


This is the handout on the PNS and Cranial nerves. See course outiline. Peripheral Nervous System (PNS) The components of the PNS include (1) nerves, (2) ganglia, and (3) receptors. Cranial Nerves chapter 14 p 477 table 14.3 p 485-489 Twelve pair of cranial nerves branch from the human brain. For each cranial nerve you must know the Roman numeral, name, whether it is sensory (S) or motor (M) or both (B)(mixed), and function. Name S, M or B Function I Olfactory S smell II Optic S vision III Oculomotor M eye muscles IV Trochlear M eye muscles V Trigeminal B S - face, teeth & scalp, M - facial muscles VI Abducent M eye muscles VII Facial B S - taste & tongue, M - pharyngeal muscles (swallowing) VIII Vestibulocochlear S hearing & equilibrium (Auditory) IX Glossopharyngeal B S - taste & tongue, general sensation of pharynx

M - pharyngeal muscles (swallowing) X Vagus B S - visceral sensation

M - visceral movement including phonation by larynx (speech)

*great distribution leads to many visceral functions XI Accessory M swallowing, head and shoulder movement XII Hypoglossal M tongue - speech & swallowing


Electrical Properties of Cells Electrical potential If you were to stick an electrode into any cell of the body and compare it to the outside of the cell you would be able to measure an electrical potential. ECF ++++ Volt meter

- 70 mV

ICF ----- fig. 12.9 p 397 This electrical potential is produced by differences in concentration of ions (ion imbalance) on either side of the cell membrane. Although many different ions are found in the ECF and ICF, the resting potential is determined mainly by 2 cations: K+ and Na+. More on this later. The lipid bilayer acts as an effective insulator. Your textbook calls this a membrane potential. The electrical potential may be measured in voltage. Current (I) = voltage(V)/resistance (R) I = V/R: this is Ohm’s law. Or V= I x R

• Current = the movement of ions across the membrane. • Resistance = the cell membrane resisting the movement of ions. • Voltage is the potential energy between the interaction of the ion flow

through the cell membrane. A greater difference between positive outside ions and negative inside ions will create more potential current flow (more voltage). If the membrane resistance to ion flow is lowered, more current will flow. If the positive and negative ions are in balance on each side of the membrane, the voltage is zero (0).


Since such small amounts of electricity are involved the voltage is measured in millivolts = 1/1000th of a volt. By convention, the voltage inside the cell (intracellular fluid ICF) is compared to the voltage out the cell (extracellular fluid ECF). Fig. 12.10 p.398

• At rest there are more positive ions just outside the cell membrane than inside so the resting potential of the cell is given as negative voltage ( average -70 mV, range –40 to –90 mV).

Mechanisms of Establishing Membrane Potentials There are 2 basic processes that may lead to unequal distribution of charges ( charge gradient, ion imbalance) on either side of the cell membrane: 1. Differential permeability of membranes to specific ions. 2. Active transport (Na+/K+ pump). 1. Differential Permeability of Membrane.

• The leakage occurs through protein channels along the membrane that are always open.

o Therefore they are called leakage or nongated ion channels. o The major cations involved here are sodium (Na+) and

potassium (K+). • The cell membrane has more K+ than Na+ leakage channels and is

therefore more permeable to K+ than Na+. o Permeability of K+ is 50 -100x > Na+. o Therefore, Na+ ions are found primarily outside the cell. o K+ ions are found primarily inside the cell but tend to leak out

due to diffusion through the “leaky” membrane. o It is due to the leakiness of the K+ ions that the inside of the cell

membrane is less positive and said to be slightly negative. • Note that the large anionic proteins cannot leave the cell and

contribute to the negative charge at the inner membrane. Fig. 12.9, p.397


Na+ positive outside + + + + + + + +

K+ Cell

- - - - - - - - - - - - Less positive inside Or ‘negative’ side Cell

• K+ ions can’t leak out forever. K+ ions flow down their concentration (chemical) gradient, outside the cell.

• But the increasingly negative charge (electrical) difference starts to pull K+ back into the cell and a balance is reached at about –90mV.

o This is called the potassium equilibrium potential. o Note that K+ moves down its concentration gradient but against

its electrical gradient. o Since the outside ECF membrane is positive, the K+ ions are

repelled.

• The majority of the resting membrane potential is due to potassium leakage.

• By itself, the membrane potential would be about –90 mV. • The resting membrane is modified to about –70mV as Na+ ions flow

across the membrane at slower rates in the opposite direction and the Na/K pump expels more Na ions than K ions are move inside (3:2 ratio).

• Even though the Na+ leakage is slow, there is no gradient to oppose

it (electrical or chemical), and it would destroy the electrochemical gradient.

o Note that the Na+ ions move down a chemical and electrical gradient.

o The inside ICF membrane is negative so the Na+ ions are attracted.

• Now, there must be a way to establish the high Na+ in the ECF and

the high K+ in the ICF that allows for this membrane potential to be established.

2. Active Transport: the Na+/K+/ATPase pump.


There are many active transport pumps in the membrane that move K+ and Na+ against their chemical gradients. ATP is expended to create these concentration gradients. Fig. 3.11 p. 70.

• The Na+/K+ pump serves to move K+ ions into the cell and to pump Na+ ions out of the cell.

o It requires ATP to configure the protein to act as a pump. o For every 3 Na+ ions moved out, 2 K+ ions are moved in.

• Since K+ diffuses out of the cell easily, the net effect of the pump is to remove Na+ from the cell.

• There are 100’s of these pumps per um2 of cell surface. • The combination of the passive forces of diffusion through a

semipermeable membrane (leaky channels) and the active force of active transport Na+/K+ pump), there is an unequal distribution of ions leading to a membrane potential.

• This type of membrane potential is called a resting potential as the nerve cell is at rest. It remains this way as long as there is no stimulation.

The membrane is said to be polarized. ECF + + + + + + + + + + + + + + + + + + + + + + + + + + + + + - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -Cell ECF + + + + + + + + + + + + + + + + + + + + + + + + + + + + +

Resting nerve cell or fiber, with a polarized membrane. As a side note, the primary task of the Na/K pump is to control water concentration in animal cells. As proteins and other biomolecules are manufactured inside the cell, the cell may become hypertonic. As a result, water will enter the cell. In animal cells with no cell wall to protect against the cell bursting as water moves in by osmosis, Na is pumped out and the water will follow. Remember that the cell membrane does not allow much Na to enter back into the cell while K can move quickly back out through membrane channels that are normally open. Nerve Impulse and Action Potential Now, we will compare the resting nerve cell with a stimulated nerve cell.


Action Potential (AP)- the action potential will be described in 2 steps: Step 1. The cell membrane becomes highly permeable to Na+ and depolarizes. Fig. 12.12,steps 1-2 p.401

• When the membrane is stimulated (during nerve excitation) it becomes highly permeable to Na+.

• Na+ rushes into the nerve cell due to the concentration gradient and the membrane is depolarized leading to an action potential.

• Na+ enters the nerve cell membrane through special ion channel proteins called a chemical gated channel.

o When the neurotransmitter (chemical) binds to the membrane, it opens the ‘gate’ of the protein so Na+ ions can rush in to the cell.

o This is the graded potential we previously discussed with muscle excitation. Fig. 12.14, p.405

o The Na+ rushes in due to the concentration gradient (higher to lower) and chemical gradient (opposites attract, the negative inside attracts the positive outside).

Voltage Gated Channels

• If enough Na+ enter to a threshold level (about –55 mV), then Na++ voltage gated ion channels in the membrane open to let Na+ rush in to further depolarize the membrane until it reverses to become +30 mV.

o Electrical protein gates in the membrane are very sensitive to potential changes and distortions occur that flips them to another conformation, in this case open.

o Na+ permeability is now 600x greater than K+. • As a result, further depolarization occurs opening more and more Na+

gates in a positive feedback cycle. Na Na Na + + + + + + + + + + + + + + + + + + + + + + + +

- + - - + - - + - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -


+ + + + + + + + + + + + + + + + + + + + + + + + + + + + +

Stimulated nerve cell or fiber, with a depolarized membrane. (Step 1) Step 2 Resting potential is restored = repolarization. Fig. 12.12 step 3-4. The same depolarizing event that opens the Na+ gates also triggers 2 other events:

1. The Na+ gates are triggered to close, after a few 10,000th of a second after they open.

About 20K Na+ flow thru the gate when open.

2. Voltage gated K+ channels are triggered to a delayed opening, about the time that the Na+ gates close.

• At this time voltage gated K+ channels are opened that allows increased diffusion of K+ out of the cell.

• The Na/K pump fine tunes the resting potential disrupted by the action potential.

• These events allow for the repolarization of the nerve cell membrane to the resting potential (-70 mV).

K K K + + + + + + + + + + + + + + + + + + + + + + + +

- + - - + - - + - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -

+ + + + + + + + + + + + + + + + + + + + + + + + + + + + +

Resting potential of nerve cell or fiber restored = repolarization. (Step 2) Each of these 2 events occurs sequentially along the nerve fiber = nerve impulse. The relative amount of Na/K that moves across the membrane during an AP is inconsequential to the ECF/ICF concentrations of Na/K. So, the concentration gradients are not disturbed, so repeated APs can occur as soon as the membrane is repolarized.


Propagation of Action Potential Fig. 12.13a p.403 The movement of the nerve impulse along the nerve fiber is called propagation.

• The Na+ ion rushing in moves sequentially in the direction of fewer + ions along the nerve fiber causing depolarization along the way.

o This is a domino type of effect. • This propagation along the fiber is called an impulse or conduction. • Impulses travel from the trigger zone at the nerve cell body (axon

hillock) to the axon terminals toward the next nerve cell or effector cell (muscle or gland).

o Movement is in one direction because the membrane has repolarized as soon as it passes as we previously discussed.


Graphic View of an Action Potential (Impulse) Let’s review a graphical representation of an action potential. Fig. 12.11, p.399. Depolarization repolarization potential

graded Na+ in K+ out threshold for AP (-50-55 mV)

resting potential (-70 mV) step1 step 2 hyperpolarization Stimulus Time (ms)

50 40 30 20 10

membrane 0 potential -10 mV -20

-30 -40 -50 -60 -70 -80

Effects of Chemicals and Drugs on Nerve Cell Membranes DDT (dichloro-diphenyl-trichloroethane) One of the reasons the pesticide DDT is so dangerous is that it increases the nerve cell membrane’s permeability to Na+ ions. It is a lipid soluble compound and disrupts the integrity of the membrane.

• This causes spontaneous action potentials to occur all of the time.

o This seriously disrupts nerve cell transmission of information. o This is how it kills insects! Nerves keep firing and insect is

stimulated to death. • In humans, too much DDT affects the diaphragm and may result in

respiratory arrest. o 1 billion kg produced in US alone. Takes decades to

decompose. Still produced overseas in poor countries.


Local Anesthetics Lidocaine and procaine (Novacaine) have the opposite effect of DDT. (Also Marcaine with Epi, Carbocaine)

• They serve to decrease the permeability of the membrane to Na+ and prevent action potentials.

o They act as a plug in voltage gated Na+ channels, so no propagation of the action potential along the cell.

• This serves then to “numb” the localized area. See p. 400 • Tetrodotoxin (TTX) from puffer fish works in a similar manner. • Ice can act to slow pain impulses by slowing down AP generation.

Histology (Cells) of the Nervous System p 388-390 2 major categories of cells are found in the nervous system: 1. Nerve cells (neurons) – carry impulses and are electrically excitable. 2. Glial cells (neuroglia)- do not carry impulses , not electrically excitable. We will discuss glial cells first. Glial Cells (Neuroglia): table 12.1 p.392

• These cells do not carry electrical impulses as they are not electrically excitable.

• About 9:1 ratio of glial to neurons, smaller, and make up half the mass of the brain.

• You only need to know the Schwann cell by name and its function. For the other glial cells, just know the function

There are several types of glial cells with a number of different functions.

Glial cells found in CNS: See table 12.1 p 392-3 1. Astrocytes- most abundant, nutrient providers. Link between neurons and blood vessels (part of blood-brain barrier).


2. Oligodendroglia (oligodendrocytes)- produces myelin sheaths around axons. 3. Microglia- derived from monocytes and act as phagocytes. Can migrate to area of injury and infection. 4. Ependymal- ciliated semipermeable cells lining ventricles and central canal. Makes CSF and helps it circulate. Glial Cells found in PNS: 1. Satellite cells- surrounds and supports cell bodies of neurons in ganglia. 2. Neurolemmocytes (Schwann cells)- produce myelin around axons. Similar to oligodendrocytes in CNS in function.

Some of the many functions of glial cells are as follows: 1. Supportive of neurons - a "nerve glue". Like C.T. 2. Important in neuron nutrition. 3. Synthesize myelin. 4. Phagocytic.

Most brain tumors (gliomas) arise from the actively dividing glial cells (neurons do not divide). Tumors arising from neurons can occur in young children (<4yr) when neurons are still increasing in number. Now, let’s discuss neurons. Nerve Cells (Neurons): The nerve cells serve to carry electrical impulses.

• They are electrically excitable. • Other characteristics: extreme longevity, amitotic, high metabolic rate.

Fig. 12.3 p.389. There are several structural neuron cell types (fig. 12.4 p.391) but we will discuss a generalized type. A typical neuron possesses the following characteristic features: Fig 12.3 p 389


2. nerve cell body (graded potentials (stimulus) received here) myelin node of Ranvier (neurofibral node) nucleus 4. Axon terminal 1 . dendrite synapse chemical activity here 3. axon (action potentials develop here) direction of impulse

Diagram of a typical neuron with its component parts. Generalized Nerve Cell (Neuron) Component Parts and Function

1. Dendrites a. Serve to conduct information toward the nerve cell body. b. This is the area of the nerve cell that receives input and exhibits

graded (chemically gated) membrane potential in response. c. Are typically multiple and highly branched. (Receives stimuli

from other neurons). d. Are generally shorter than axon. e. Are irregular in size (diameter).

2. Cell body (soma)- contains the nucleus of the cell and typical organelles.

a. Very active metabolically. Organized into ganglia in PNS and nuclei (gray matter) in CNS. This is where graded potential are developed.

3. Axon a. This is the conducting portion of the neuron.

i. Serves to conduct the impulse away from the nerve cell body, towards other neurons, muscle fiber, or a gland.

b. Generally single but end divides into many branches (10,000 is not uncommon) forming axon terminals. Influences other neurons or effectors (muscle, glands)

c. Longer, may be 3 feet (1 meter) in length. i. Example: from spine to toe.

d. Of uniform diameter.


The Axon structure in more detail. Myelinated Axons Fig. 12.3 p. 389 Some neurons are myelinated. p 392

• Myelin is a segmented sheath of fatty tissue (white matter) that serves to increase the speed of the nerve impulse and insulated neurons from each other.

• The amount of myelin increases from birth to maturity, so infants do not respond as quickly or as coordinated as older children.

• Each segment of myelin is produced by a single glial cell (Schwann Cell) that is wrapped around the neuron (up to 100 times).

• The areas between the myelin are known as nodes of Ranvier. • The speed of conduction is greatly influence by 2 factors:

1. Diameter of the neuron, and 2. The myelin sheath.

Saltatory Conduction fig. 12.13b p.403 1. Myelin Sheath

• The myelin causes the impulse to jump quickly from one node of Ranvier to the next instead of traveling along the nerve cell membrane by depolarization and action potentials.

• The myelin covers up the membrane so no ion leakage can occur. No voltage gates are present in the membrane at this point.

• Local current flows the 1 mm distance to the next node quickly. • At the next node, the membrane undergoes depolarization and an AP

develops to rebuild the current so it can travel to the next node. Voltage gates are in high density at the nodes. Nodes slow things down but current needs to be built back up.

• This speeds up transmission considerably, about 50x for myelinated vs. unmyelinated fibers of comparable size

In summary, the jumping or skipping of the impulse that occurs in myelinated fibers is known as saltatory conduction and carries information much faster than in nonmyelinated neurons (gray matter). 2. Diameter


• The greater the diameter of the myelinated neuron, the faster will be its velocity of conduction - up to 120 meters per second (360miles/hour) (e.g. the sciatic nerve)! Versus 0.7 m/sec for an unmyelinated fiber that may service the digestive tract.

• Larger diameter means less resistance to current just as in copper wire.

• Examples: o Senses, action muscle: Type A, 5-20 um dia. 12-130m/s (27-

280 mph) o Visceral sensory, motor: Type B, 2-3 um dia, up to 15 m/sec o Sensory heat, cold,slow visceral motor: Type C, ½ - 1 ½ um dia

½ - 2 m/sec. Multiple Sclerosis Results from a disease of the myelin sheath in CNS and spinal cord. See box, p 413 There is a progressive demyelination process (you lose the myelinated sheath).

• MS is an autoimmune disease, a disease in which a person’s own immune system produces antibodies that act against his or her own healthy body tissues.

• It may be triggered by a viral infection. It affects over 2.6 million people worldwide.

• Oligodendrocytes in CNS attacked by cytotoxic immune cells. • The loss of myelin causes a decrease in the velocity of conduction of

the nerve impulse that can greatly effect coordination. • Dx: 20-40 years old. • There is a permanent scarring of the nerve tissue (plaques and scars

form) as the myelin sheaths are attacked. • Beta interferon may help slow the disease. Steroids manage acute

attacks. Bone marrow transplants are experimental to remove cytotoxic cells.

• Clinically, multiple sclerosis symptomology includes: 1. Numbness (when sensory neurons are affected. 2. Vision loss, double vision. 3. Uncoordinated movements.

• Attacks are followed by periods of remission.


Temperature also affects the conduction of nerve impulses. • A cold pack will help relieve some pain as pain nerves are partially

blocked by the cold. Now back to the nerve cell parts and function discussion. 4. Axon terminal (terminal bouton).

• An axon terminal is the bulb shaped neuron ending. • This is the secretory or output component of the neuron. • It contains synaptic vesicles that contain neurotransmitter (chemical

messenger) that carries the nervous system message chemically from one neuron to the next.

• Message can be excitatory with ACh in NMJ or inhibitory ACh in parasympathetic synapse with heart via vagus nerve (heart slows down)

• The neurotransmitter crosses a gap between the neurons known as a synapse or from the neuron to a muscle cell across a gap known as the myoneural junction (neuromuscular junction).

table 12.3 p 408 = Summary of neuronal structure and function. Assignment Questions Chapter 12 Describe the factors that give rise to resting potential. Outline the steps in the generation and conduction of a nerve impulse.


Types of Neurons There are many different types of neurons in the body, some of which we will discuss later. For now we will limit our discussion to 3 types of neurons: 1. Afferent (sensory) neurons serve to bring the impulse or information toward the brain. 2. Efferent (motor) neurons carry information out and away from the brain. 3. Interneurons (association or connector or internuncial) connect sensory to motor neurons.

~90% of the neurons of the body are interneurons. Now we will discuss and review some terms associated with neurons. Physiological Properties of Neurons (Reviewed) Threshold

• Minimum strength (voltage) of a stimulus required to depolarize a neuron (create an AP). Fig 12.11

• This is usually about –55 mV (membrane depolarizes about 15-20 mV from –70mV).

• This point is reached by the flow of Na+ across the membrane in sufficient numbers per time.

Graded Potential

• These are the small potential changes in a local area of membrane located where dendrites and cell bodies form a junction that is caused by a stimulus, for example the binding of neurotransmitter.

• These can make the membrane more (hyperpolarized or inhibitory postsynaptic potential IPSP) or less polarized (depolarized or excitatory postsynaptic potential EPSP) fig. 12.10 p.398.

• When enough occur together at the axon hillock, they may trigger an AP that travels down the axon to the axon terminal. See summation.

• They are not triggered by voltage-gated channels as AP but by chemical, pressure, or light mechanisms.

Summation Fig 12.15 p 407 discussion 406


Two ways:

1. Temporal summation: Many subthreshold stimuli may act together in an additive way to cause depolarization. This can occur by increases the rate of stimulus (temporal summation) of a single presynaptic neuron or

2. By several presynaptic (spatial summation) neurons firing to the same postsynaptic neuron. These can be caused by combinations of EPSPs and IPSPs with the outcome of an AP determined by the presence of more EPSPs.

All or None Response p 399 The response of a neuron to a stimulus is either maximal or not at all. In other words, an action potential (AP) happens completely or not at all. If enough Na+ does no enter the cell to trigger the voltage gates, no AP will occur. Refractory Period p 400 fig 12.11 p. 399 see boxes on right side of fig.

• The refractory period is a “resting period” for the neuron following depolarization when a neuron cannot generate an other action potential.

• Following depolarization, there is a period of time called an absolute refractory period during which a second stimulus, no matter how strong, will not elicit a response on the part of the neuron.

• The Na+ and K+gates are open or inactive, so repolarization is not completed.

• In large diameter axons this period is 0.4ms, 4ms in smaller axons. • In normal body conditions, maximum frequency of nerve impulses in

different axons is usually ranges from 10-1000/sec. Adaptation (Accommodation) p. 502

• A continuous stimulus over and over eventually causes a rise in threshold of the neuron; therefore it takes a greater stimulus to elicit a response.

• The receptor neuron decreases its firing rate over time with the same stimulus.


• Receptors for touch adapt quickly (so you are not aware of your clothes). Temperature receptors adapt between 20-40C but outside this range do not adapt as the risk of tissue injury is substantial.

• Joint and muscle receptors adapt more slowly. • Pain receptors do not generally adapt due to the survival value of

pain. • In laymen’s terms there is a “deadening of the nerve”. • Synonyms for accommodation would be habituation and tolerance. • Other Examples

o For example, constant repeated exposure to a specific drug, alcohol, or even noise may cause, in time, a reduced effect of that stimulus.

o In other words, to achieve the same “high”, you may need more of a specific drug.

The Nervous System Message The nervous system message is electrochemical in nature.

1. The nerve impulse passes through the neuron as an electrical message, and

2. Across the synapse as a chemical message.

• The chemical that carries the message across the synapse = neurotransmitter.

• The nervous system message travels along distinct pathways = nerves.

o (Unlike endocrine system where message travels via blood). • A nerve is a bundle of neurons (actually bundle of axons or dendrites)

bound together by C.T. like the wire strands in an electrical cable. The Synapse Fig. 12.14 p.405 Although there are electrical synapses between cells in the cardiac muscle, and some smooth muscle and CNS, we will only discuss the chemical synapse found in most nerve to nerve (muscle) contact. The Chemical Synapse


• The synapse is an area of functional but not anatomical (structural)

continuity between one neuron and another. o Therefore there is no structural connection.

• The synaptic cleft forms a chemical bridge 20-50 nm wide. • The neurotransmitter serves to functionally connect the presynaptic

neuron to the postsynaptic neuron as it diffuses across the synapse. • An AP triggers the opening of voltage Ca++ gates in the axon terminal

that triggers the exocytosis of neurotransmitter vesicles.

Physiological Properties of the Synapse 1. One way conduction

• Because only one end of the neuron contains synaptic vesicles with neurotransmitter, the chemical message can only travel from the axon terminal of the presynaptic neuron to the dendrites of postsynaptic neuron.

See text p. 406 for next 2 terms. Also fig 12.10 2. Pre synaptic Facilitation or excitatory postsynaptic potential (EPSP)

• When an excitatory presynaptic neuron synapses with a postsynaptic neuron that causes depolarization.

o The release of excitatory neurotransmitter to the postsynaptic neuron excites the membrane and cause the membrane potential to move towards 0mV (more positive) so it moves the potential closer to triggering an action potential.

o This usually caused by a Na+ channel opening in the membrane.


3. Presynaptic Inhibition or inhibitory postsynaptic potential (IPSP) • When an inhibitory presynaptic neuron synapses with a postsynaptic

neuron that causes hyperpolarization. • Inhibition is the opposite of facilitation.

o The neurons is releasing an inhibitory neurotransmitter causing further hyperpolarization of the membrane.

o This usually caused by opening a K+ or Cl- channel. o The subtracts from any graded potential produced by a

excitatory synapse. It competes against an excitatory neuron to create an action potential

o So, a greater excitatory stimulus is necessary for the message (AP) to continue.

• Presynaptic facilitation and inhibition effects can last for minutes to hours.

• They are of interest in terms of learning and memory. Fig. 12.15 p.407 4. Summation

• Summation occurs when: o Many presynaptic neurons converge on a single postsynaptic

neuron (spatial summation) or o A single presynaptic neuron repeatedly fires in rapid succession

(temporal summation). • You may have many subthreshold stimuli that work in an additive way

to produce enough neurotransmitter to meet the threshold of the postsynaptic neuron.

o Example: The typical CNS neuron receives input from 1000-10,000 synapses.

5. Synaptic delay p 405

• The speed of the nervous system message slows at the synapse because the electrical AP is converted to a chemical signal (neurotransmitter) and then back to an AP.

• This is about a 0.5 ms delay. • The velocity of the electrical message may be as high as 120 meters

per second along the neuron but chemical message slows to 0.5-1.0 ms at the synapse.

• Therefore the fewer the number of synapses to get the message from one place to another, the faster it will travel.


Other synapse notes

• Many drugs have great effect on the synapse; we have discussed some of these.

o Aspirin causes sensory (pain) inhibition by raising the threshold of conduction of impulses near the hypothalamus (pain center).

• pH o Increased pH (basic condition, alkalosis) serves to increase the

ease of transmission, while lowering the pH (acidic condition, acidosis) serves to depress transmission.

• O2 Hypoxia (low oxygen levels) can lead to cessation of synaptic activity.

Types of Neurotransmitters These are discussed in text p.407-410

• Neurotransmitters are present throughout the PNS and CNS. • They may be inhibitory, excitatory, or both, depending on the

receptor! • Some act on the membrane directly to open ion channels

while other activate secondary messenger systems in the membrane that influence reactions inside the cell.

• About 100 are known. Examples of neurotransmitters from the body follows: 1. Acetylcholine (ACh)

• Very common throughout the body as already discussed and is continually broken down by acetylcholine esterase (AChE).

• Excitatory in neuromuscular junctions, but in inhibitory at parasympathetic heart synapses.

Biogenic amines are certain amino acids that are modified and decarboxylated. Depending on the receptor for these, they can be excitatory or inhibitory. Examples: 2. Norepinephrine (NE) Derived from tyrosine.

• Found in CNS for roles in arousal from sleep, dreaming, mood.


• Found in the PNS (postsynaptic neurons of the sympathetic division of the nervous system). Also a hormone secreted from the adrenal medulla to fortify a sympathetic response via the vascular system.

• Can be excitatory or inhibitory depending on receptor. • The chemical structure of amphetamines is similar enough to mimic

norepinephrine. o Therefore when a person takes amphetamines they exhibit a

sympathetic nervous system response that includes increased heart and respiratory rate, dilated pupils, etc.

• Unlike acetylcholine that is continually broken down by acetylcholine esterase, norepinephrine is removed from the receptor sites and transported back across the synapse and back into the synaptic vesicles to be used again and again.

o Cocaine is a drug that blocks the transport of norepinephrine (and dopamine) back across the synapse.

o Therefore it makes sense that a person under the influence of cocaine will exhibit a sympathetic nervous system response.

3. Serotonin (5-hydroxytryptamine (5-HT)) made from tryptophan (amino acid)

• Found in the CNS involved in mood control, appetite, sleep induction, temperature regulation.

• Serotonin is a neurotransmitter involved with behavior and has been implicated in many psychotic disorders including depression and others with hallucinatory symptoms.

• People with depression exhibit serotonin deficiency and schizophrenia exhibit high levels (or dopamine too).


o Prozac (fluoxetine), a commonly used antidepressant, is known to inhibit serotonin reuptake and more is available in the synaptic cleft.

• Mescaline, a drug found in peyote cactus, and LSD are known to block serotonin receptor sites therefore bringing about hallucinations.

5. Amino acids Several amino acids are neurotransmitters in the CNS. Can be excitatory (glutamate) or an inhibitory neurotransmitter in the CNS. Example of inhibitory: GABA (Gamma Amino Butyric Acid)

• Found only in brain. Most common inhibitory neurotransmitter, in as many as 1/3 of all brain synapses.

• It has a tendency to increase the cell membranes permeability via chemically gated Cl- channels (as opposed to Na+ ions).

• This makes the cell membrane even more polarized and therefore less excitable (inhibition). Antianxiety drugs diazepam (Valium) enhances these effects.

• It is augmented by alcohol (slowed reflex coordination) and Valium.

Endorphins: concentrated in pituitary, thalamus, hypothalamus. Natural opioid peptide. Relieves pain by inhibiting release of P substance from sensory nerves. Tetanus toxin (produced by bacteria introduced into a wound) prevents the release of inhibitory neurotransmitters in neurons allowing all muscles to contract simultaneously leading to a condition we call tetanus (lockjaw). See table 12.3 p.408 for review of neuron structure and function Components of a Spinal Reflex Arc


fig. 13.5 p.427

• A reflex is a very fast involuntary response that serves to prevent bodily harm.

• Said another way, they are programmed, stereotyped, predictable motor responses to specific sensory stimuli.

• These make up the behavior of simpler animals. • There are few synapses and the message only has to travel to the

spinal cord (not the brain) for you to respond, therefore your response is very quick.

o Many brain reflexes exist (eye movement, sneeze, etc., but we will not discuss)

Example: Jerking your hand back from a hot flame. A withdrawal reflex or a limb flexor reflex. Fig 13.8 p 431

1. Receptor - a sense organ detects a stimulus (heat receptor in this case).

2. Afferent neuron - serves to carry the information to the spinal cord (integrating center).

3. Interneuron - is found within the spinal cord and connects the afferent (sensory) neuron to the efferent (motor) neuron.

a. This is the integrative function leading to the stimulation of the flexors.

4. Efferent neuron - carries the motor information from the spinal cord to the effector organ in the periphery.

5. Effector organ - a motor effector (skeletal muscle in this case) that contracts and causes you to jerk your hand back.

Questions Chapter 12 Describe presynaptic facilitation and inhibition. Describe spatial and temporal summation. Chapter 13 What is a reflex arc? List and define the components of a reflex arc and describe how the spinal cord serves as an integrating center for reflexes.


The Central Nervous System The Brain Development of the Brain Text p 490-491 Fig. 14.25 p.490

• The nervous tissue begins as a thickening of the embryonic ectoderm that forms a neural plate.

o The plate rounds to form a groove. o As the edges of the groove meet they form the first early

structure, a tube. o So, brain begins as a simple tube, a neural tube.

• The tube or chamber (ventricle) is filled with cerebrospinal fluid. o The cerebrospinal fluid serves to cushion the brain and spinal

cord.

Nervous tissue

Chamber (ventricle) filled with fluid called cerebral spinal fluid. CSF serves to cushion brain.

View a 3-4 week embryo brainFig. 14.26a left, p.491 See an early CNS with forebrain, midbrain, and hindbrain, with the spinal cord descending.

• With time we see further development of the brain and can see the major brain divisions (primary vesicles) begin to appear. Soon, the:

o Forebrain (proencephalon), o Midbrain (mesencephalon), and o Hindbrain (rhombencephalon) become apparent.

View a 5- week old embryo brainFig. 14.26b p.491. See where the subdivisions of the brain develop. As development proceeds, these 3 fluid filled vesicles undergo further bending and constriction forming 5 secondary vesicles as follows: 1. Forebrain (Prosencephalon) becomes the telencephalon and

diencephalon. a. The telencephalon will become the cerebrum (2 hemispheres, basal

ganglia (nuclei), 2 lateral ventricles).


b. The diencephalon will become the thalamus (3rd ventricle), and

hypothalamus. 2. Midbrain (mesencephalon) becomes the mesencephalon (with cerebral

aqueduct). 3. Hindbrain (rhombencephalon) becomes the metencephalon and

myelencephalon. a. The metencephalon becomes the pons, and cerebellum. b. The myelencephalon becomes the medulla oblongata.

Use fig. 14.1 p. 453 See a developed brain With greater development, we begin to see extensive convolutions of the cerebrum above, and the cerebellum below. This folding allows for more neurons to fit is a limited space (the skull). Formation of the Spinal Cord

• The neural tube inferior to the myelencephalon becomes the spinal cord.

• 2 neural tube defects, spinal bifida (lack of closure of the vertebrae) and anencephaly (absence of skull and cerebral hemispheres) are associated with low levels the B vitamin folic acid.

o So, folic acid supplements are important for a healthy pregnancy.

Component Structures of the Brain figure 14.1 p. 453 table 14.1 Telencephalon Cerebrum p. 467 Function The cerebrum perceives information, directs motor responses, and, is the center of intellect, memory, language, and consciousness. Structure The cerebrum is subdivided by convolutions. Fig. 14.11 p.468 In terms of the convolutions:

• Grooves or depressions are called a sulcus (sulci) or fissure.


• Rounded or elevated portions of the convolutions are called a gyrus (gyri) .

• It is important to note that the convolutions are not a random pattern. • The longitudinal fissure divides the cerebrum into right and left halves

called cerebral hemispheres. o Within each of the hemispheres, the fissures divide the

cerebrum further into lobes. • The lobes of the cerebrum are located on its outer surface known as

the cerebral cortex. • The cerebral cortex is the gray matter of the cerebrum. An outer rim

(2-4 mm) of gray matter. • It consists of approximately 12 to 15 billion nonmyelinated neuron cell

bodies and associated glial cells. • The gray matter is the computer of the CNS and the white matter the

wires that interconnect the computing areas. • The cerebrum accounts for 80% of the brain weight and the human

cerebrum is the most developed of all species. Lobes of the Cerebral Cortex Fig. 14.11 p.468 The lobes of the cerebral cortex are named for the bones of the cranium that overlay them. Note locations on fig. 14.11 Functions: Fig. 14.15 p. 474 1. Frontal Lobe

• The frontal lobe is a primary motor area, also known as the somatomotor area. Fig 15.5 p. 508.

o It is responsible for voluntary movement. See the primary motor (#4), area located in the precentral gyrus. Note: ALS (amyotrophic lateral sclerosis, Lou Gehrig’s disease) attacks this area, as well as the lateral white columns, and lower motor neuron cell body’s.

• It is also responsible for speech in part (Broca’s area (#44)). • It is separated from the parietal lobe by the central sulcus. • It is separated from the temporal lobe by the lateral cerebral sulcus.


2. Parietal Lobe • The parietal lobe is a general sensory area.

o Examples: touch, pressure, heat, cold, pain. • It receives and processes sensory input. Fig 15.5a • Therefore it is completely afferent in its function. • It is separated from the occipital lobe by the parieto-occipital sulcus.

3. Occipital Lobe

• The occipital lobe is primarily responsible for processing visual input or vision.

• It is sometimes called the visual cortex. 4. Temporal Lobe

• The temporal lobe is the auditory area where sound sensation is received and associated with speech, music, or noise.

• It is of primary importance for hearing and some speech. • It is sometimes called the auditory cortex.

As stated earlier, the fissures that can be seen on the lobes of the cerebral cortex are not a random pattern.

• The fissures serve to separate areas of the brain with different functions.

• About 100 different functions have been isolated for different convolutions of the brain.

How was this determined?

• This was originally done by inserting electrodes into different parts of the brain and monitoring the activity of the brain.

• Also, people with specific brain damage have provided invaluable information.

• New equipment, is less invasive. o MRI with computers can now monitor the slight temperature

changes that take place in the brain as blood flows into areas that become active during different activities.


White Matter of the Cerebrum P 469 The white matter of the cerebrum is located beneath the cerebral cortex. It consists largely of myelinated fibers bundled into large tracts.

• They functions as wires that allow interaction between parts of the cerebral cortex or other areas of the brain.

• This integration is essential for even the simplest of tasks. • Example: picking a flower and enjoying (vision, fragrance, movement,

beauty, etc) They are organized into tracts and are classified according to which direction they run into of 3 types of fibers: Fig. 14.12 p.408 1. Commissural Fibers Structure: Commissural fibers serve to connect the corresponding areas of the 2 cerebral hemispheres (right and left brains). Example: Fig 14.9 p 469

• The largest structure they comprise is called the corpus callosum. Function:

• Coordinates actions on both sides of the body. 2. Projection Fibers Structure:

• These fibers form ascending and descending (vertical) tracts that connect the cerebrum to the lower brain, spinal cord.

• Example: See the Internal Capsule just lateral to the thalamus, which then continues as the corona radiata to the cortex. fig. 14.13b p.470.

• Also see projection tracks. Fig 14.2 p469 Function:

• Projection fibers serve to connect the cerebral cortex to the lower brain and spinal cord. They tie the cerebrum to the rest of the nervous system and to the receptors and effectors of the body.


3. Association Fibers Structure:

• These tracts connect gyri within a hemisphere. • Short fibers connect adjacent gyri and long fibers connect different

cortical lobes. • Example: Association fibers. Fig 14.12

Function: • Transmit impulses between gyri in the same hemisphere. • One role is to link perceptual and memory centers, so you can

associate a smell with a thing. Basal Ganglia (nuclei) P 469-71 Fig. 14.13 p.470 The deep area of white matter of the cerebrum also contains several groups of nuclei called the basal ganglia (3 masses of gray matter in each hemisphere). Function:

• Regulates motor functions executed by the cortex, regulates muscle tone, and coordinates rhythmic movements (e.g. arm swinging while walking).

• Important in starting and stopping movements and the intensity of movement.

• Other functions too related to cognition and emotions. Parkinson’s disease p 515, 521

• The basal ganglia cells that degenerate have been implicated in Parkinson’s disease also known as shaky palsy.

• The loss of dopamine releasing cells in the basal nuclei causes an increase in tone.

• Parkinson’s disease appears in people in the age group of 50 to 65 and causes tremors of the limbs, slow movements, and postural changes (stiffness of face, arms, and legs).

• It may be caused by environmental toxins or pesticides. Huntington’s disease p 515


• An inherited (autosomal dominant) condition, causes overstimulation of the motor drive.

• Loss of neurons in the basal ganglia that release GABA or ACh. • Key sign is chorea: Limbs jerk unstoppably in a dance like manner. • Onset at 30-40, then death within 10-20 years.

Asymmetry of the Brain or Brain Lateralization p. 475-476 table 14.2 p. 477

• The brain can be thought of as 2 hemispheres connected by a bundle of nerve fibers called the corpus callosum (commissural fibers).

• Sensations from one side the body are most commonly perceived in the cerebral hemisphere on the opposite side of the body.

• Example: Vision of the left eye is controlled by the right hemisphere, and vice versa.

The 2 cerebral hemispheres are asymmetrical in some structure and function.

• If the left temporal lobe of the brain is damaged, you will commonly observe language difficulties.

o If the right temporal lobe is damaged, there are no such difficulties.

• In dyslexia (difficulty in reading), the left temporal lobe is typically smaller than a right.

• The 2 hemispheres of the cerebrum have the following

responsibilities: Left hemisphere Right hemisphere Speech Visual -- spatial relationships Language Dreaming/imagination Analytical problem solving Musical and artistic ability Control of right side Control of left side

• A right handed person will have a larger left temporal lobe, left occipital lobe, and right frontal lobe.

o 90% of people are left hemisphere dominant. • A left handed person usually has right hemisphere dominant of no

asymmetry (may be ambidextrous).


Diencephalon — thalamus and hypothalamus Thalamus P 464-465 fig. 14.9. p.464.

• It is composed of paired oval masses of gray matter organized into nuclei.

• The thalamus is a relay center for sensory information received from the spinal cord, cerebellum, and brain stem going to the cerebrum.

• It can crudely sense pain, temperature, and pressure. • It plays an important role in cognition: awareness and acquisition of

knowledge. • Epithalamus:

o Superior and posterior to the upper portion of the thalamus is the epithalamus that contains the pineal gland.

o The pineal gland secretes melatonin, a hormone, and controls sleepiness and biological rhythms (biological clock).

Hypothalamus P 466-467 fig. 14.10 p.466.

• The hypothalamus is a collection of nuclei and associated fibers that lie beneath the thalamus.

• The hypothalamus is extremely important. • It is an integrating center for important homeostatic functions and

serves as an important link between the autonomic nervous system and the endocrine system.

• It secretes several hormones that influence the pituitary gland. • Many axons extend to sympathetic and parasympathetic nuclei in the

brain stem and spinal cord. It controls many vegetative (or visceral) functions (regulation of the internal environment).

• That is, functions not under voluntary control. • In other words, these things happen without thinking of them (you are

vegetating!) • The hypothalamus is of primary importance in the maintenance of

homeostasis. Functions of Hypothalamus:


1. Control of the pituitary gland, the master gland of the endocrine system.

2. Body temperature regulation via ANS. 3. Control of appetite (food intake). 4. Water balance (urine output via ADH secretion) and intake (thirst). 5. Controls and integrates activities of the ANS. Main regulator of

visceral activity. Examples: Gastric secretion, heart rate, GI food movement

The hypothalamus is also involved in emotion as a part of the limbic system. fig 14.14 p 471

• The limbic system or the ‘emotional brain’ is important in the expression of fear, rage, aggression, pain, pleasure, and instinctual sexual behavior. It is located encircling the brain stem and corpus callosum.

• The limbic system has special neurotransmitters called endorphins that are natural opiates that lessen pain and stress.

• Its evolutionary age (600 million years) is much older than the cortex (60 million years).

Now, on to the brain stem (midbrain, pons, and medulla) Most of the cranial nerves arise from the brain stem. Mesencephalon or midbrain P 460-462 Fig. 14.7 p.461 The midbrain serves a relay center between the forebrain and hindbrain. Contains the cerebral aqueduct which connects the 3rd and 4th ventricles. Several reflexes are controlled here. Examples: Eye, head, neck movements in response to visual and other stimuli. Metencephalon — Pons and Cerebellum Pons P 459-460 fig. 14.8c p.463.

• The pons lies directly superior to the medulla and anterior to the cerebellum.

• It has both nuclei and white matter. • It acts as a bridge connecting the spinal cord with the upper brain.


• It helps control breathing with the hypothalamus. • The pons also relays motor information from the cerebrum to the

cerebellum. Cerebellum P 462-463 fig. 14.8 p.463

• The second largest portion of the brain and lies in the inferior and posterior area of the cranial cavity.

• The cerebellum is the center for motor coordination of complex body movements. It evaluates how well movements initiated by the cortex are actually being carried out.

o It compares the motor output from the cortex with the sensory input from proprioceptors in muscles, tendons, and joints, and receptors for equilibrium and vision.

o The cerebellum sends feedback to the motor area to correct activity of skeletal muscle.

• It is also important in maintaining equilibrium (balance) and in the coordination of antagonistic muscles (posture).

• So, it makes possible all skilled motor activity: dancing, catching a ball, etc.

Myelencephalon — Medulla oblongata p. 458 Fig 14.6 p 460

• The medulla oblongata is continuous with the spinal cord and begins at the foramen magnum and ends at the pons (about 3cm). Sometimes called the brain stem.

o However, the brain stem includes the midbrain, the pons, and the medulla oblongata.

• The medulla oblongata serves to regulate some vital and nonvital body functions.

Vital functions Nonvital Functions Respiration center (breathing rhythm) Sneezing Heart rate and force (cardiac center) Coughing Blood vessel diameter (vasomotor center) Vomiting Swallowing Hiccuping Blows to the back of the head or upper neck can be fatal due to the vital activities of the medulla.


• The medulla oblongata is where the crossing of fiber tracts (decussation) takes place and is responsible for the right side of the brain controlling what takes place on the left side of the body and vice versa. About 90% of the fibers cross here.

Reticular formation P 462

• The reticular formation is found within the brain stem and regulates consciousness, that is, whether you are awake, sleeping, or dreaming. Fig 15.10 p518

• It is a located throughout the brain stem where white and gray matter are interspersed in a net like configuration.

• It alerts the cerebral cortex to incoming sensory signals. o This is called the reticular activating center (RAS). P. 517 o It is responsible for maintaining consciousness and awakening

from sleep by arousing the cortex. o The RAS responds to incoming impulses: ears (alarm clock),

eyes (light of morning), or painful stimuli that arouse the cortex. Note: no olfactory input so may be over come by smoke in sleep. Therefore, have a smoke detector in sleeping areas.

• The main descending function is maintenance of muscle tone. Consciousness, emotions, learning and memory. We will leave these topics for your psychology class! Found in chapter 15 p. 519-520 if interested. Blood supply to the brain. p. 492 A cerebrovascular accident (CVA) occurs by:

1. Ischemic event, or 2. Hemorrhage due to vessel rupture.

Will appear as an abrupt onset of neurological deficits such as paralysis or loss of sensation. We will discuss this in more detail with the cardiovascular system discussion. Exam II Multiple choice 50 pts Matching 10 pts 3 essay 3x5= 15 pts 75 total points


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