this chapter is about introducing the function of neurons ◦ how they conduct & transmit...
TRANSCRIPT
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Ch 4: Neural Conduction & Synaptic Transmission
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This chapter is about introducing the function of neurons◦ How they conduct & transmit electrochemical
signals through the nervous system
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Function of neurons centers around the membrane potential◦ The difference in electrical charge between the
inside & outside of the cell Can measure membrane potential using a
microelectrode◦ Measure the charge inside the cell & the charge
outside.
Resting Membrane Potential
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A neuron’s resting potential is -70mV◦ Meaning, the charge inside the cell is 70mV less
than the charge outside◦ Inside < Outside
Because this value is beyond 0, it is said to be polarized
So at rest, neurons are polarized.
Resting Potential
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It is polarized due to the arrangement of ions◦ The salts in neural tissues separate into + and –
charged particles called ions 4 main ions are responsible:1. K+ (potassium)2. Na+ (sodium)3. Cl- (chloride)4. - charged proteins
Ionic Basis
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The ratio of – to + ions is greater inside a neuron than out, so you have a more – charge inside◦ Again, why the neuron’s resting potential is
polarized 2 things cause this imbalance & 2 things try
to equalize (homogenize)
Ionic Basis
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Equalizers (homogenizers)1. Random motion2. Electrostatic pressure Cause imbalance1. Passive flow2. Active transport
Contributing Factors to Resting Potential
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1. Random Motion Ions are in constant random motion Tend to be evenly distributed because
they move down their concentration gradient
◦ Move from areas of higher concentration to lower concentration
2. Electrostatic Pressure Ions with the same charge will repel each
other Opposite charges attract
Equalizers
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Concentrations of Na+ and Cl- are greater outside the neuron (extracellularly)
K+ concentration is greater inside the cell (intracellularly)
Negatively charged proteins generally stay inside the neuron
Contributing Factors to Resting Potential
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1. Passive Flow◦ Does not require energy◦ The membrane is selectively permeable to the
different ions K+ and Cl- ions easily pass through the membrane Na+ ions have difficulty passing through
◦ Ions passively flow across the membrane via ion channels
Special pores in the membrane
2. Active transport◦ Needs energy to power the pumps
Imbalance…rs
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2. Active transport◦ Requires energy to power the pumps that
transport the ions◦ Discovered by Hodgkin & Huxley
Nobel prize winning research Why is there high Na+ and Cl- outside and high K+
inside? Why are they not passively flowing down their concentration gradients & reaching equilibrium?
Calculated the electrostatic pressure (mV) that would be necessary to counteract the passive flow down the concentration gradient (aka keep the concentrations uneven across the membrane) & how this differed from the actual resting potential
Imbalance…rs
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Discovered that there are active pumps that counteract the passive flow of ions in & out of the cell (specifically for Na+ and K+)
Sodium-potassium pumps◦ Actively (using energy) pumps Na+ out & K+ in◦ 3 Na+ ions out for every 2 K+ ions pumped in
Other types of active transporters also exist
*Summary Table 4.1 (pg. 79)*
Active pumps cont.
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Remember: At a synapse, the presynaptic neuron releases NT that bind with receptors on the postsynaptic neuron, to transmit the signal from one neuron to the next
When the NT bind with the postsynaptic neuron, they have either of 2 effects
1. Depolarize the membrane◦ Decrease the resting potential◦ **this means become less negative, aka approach zero**
2. Hyperpolarize the membrane◦ Increase the resting potential◦ ** make it more negative; further from zero**
Postsynaptic Potentials
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-70 MV
0 MVhyperp
ola
rize
depola
rize
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Postsynaptic depolarizations:◦ Excitatory postsynaptic potentials◦ EPSPs◦ Increase the likelihood that the neuron will fire
Postsynaptic hyperpolarizations:◦ Inhibitory postsynaptic potentials◦ IPSPs◦ Decrease the likelihood that the neuron will fire
Graded responses◦ Weak signals cause small PSPs; strong signals
cause large PSPs
Postsynaptic Potentials
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Travel passively◦ Very rapid (practically instantaneous)
Like a cable◦ Deteriorate over distance
Lose amplitude as they go along Fade out Like sound
PSPs
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Individual PSPs have almost no effect on getting a neuron to fire
However, neurons can have thousands of synapses on them & combining the PSPs from all of those can initiate firing◦ Called integration◦ Add all the EPSPs + IPSPs◦ Remember:
PSPs are graded & have different strengths ExcitatoryPSPs increase the likelihood of firing &
InhibitoryPSPs decrease the likelihood
Integration of PSPs
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Neurons integrates PSPs in 2 ways
1. Over space: spatial summation
◦ EPSP + EPSP = big EPSP◦ EPSP + IPSP = 0 (cancel each
other out; assuming of equal strength)
◦ IPSP + IPSP = big IPSP
2. Over time: temporal summation
◦ 2 PSPs in rapid succession coming from the same synapse can produce a larger PSP
Integration of PSPs
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If the sum of the PSPs reaching the axon hillock area at any one time is enough to reach the threshold of excitation, an action potential is generated ◦ The threshold is -65mV
So the resting membrane potential must be depolarized 5mV for the neuron to fire
Action potential◦ Massive, 1ms reversal of the membrane
potential -70 to +50mV
◦ Not graded; they are all-or-nothing responses Either fire at full force or don’t fire at all
Action Potentials
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APs are generated & conducted via voltage-activated ion channels
When the threshold of excitation is hit, the voltage-activated Na+ channels open & Na+ rushes in
The Na+ influx causes the membrane potential to spike to +50mV
This triggers the voltage-gated K+ channels to open & K+ flows out
After 1ms, Na+ channels close End of rising phase
Conduction of APs
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Beginning of repolarizing phase◦ K+ continues to flow out until the cell has been
repolarized; then the K+ channels close Cell returns to baseline resting membrane
potential
Conduction of APs cont.
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Refractory Periods For about 1-2ms after the AP, it is
impossible to fire another one◦ Absolute refractory period
Followed by a period during which another AP can be fired, but it requires higher than normal levels of stimulation◦ Relative refractory period
Afterwards, the neuron returns to baseline & another AP can be fired as usual
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Ions can pass through the membrane at the nodes of Ranvier between myelin segments
APs move instantly through myelinated segments to the next node, where concentrated Na+ channels allow the signal to be “recharged” and sent to the next
Conduction in Myelinated Axons
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Saltatory Conduction Overall, this allows APs to be conducted much
faster than in unmyelinated axons, because the AP “jumps” from node to node and effectively “skips” the lengths covered in myelin (saltatory conduction)
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Speed of conduction is faster with myelin Faster in thicker axons Ex: mammalian motor neurons are thick &
myelinated & can conduct signals at around 224 mph!!
Velocity of Axonal Conduction
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Different types of synapses based on the location of the connection on each neuron◦ Axodendritic
“Normal” synapses Terminal button of axon on Neuron1 to
dendritic spine of Neuron2◦ Axosomatic
Axon of N1 to soma of N2◦ Dendrodendritic◦ Axoaxonic
Structure of Synapses
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2 categories of NTs◦ Large:
Neuropeptides◦ Small:
Made in terminal buttons & stored in vesicles
Neurotransmitters
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NTs are released via exocytosis At rest, NTs are in vesicles near membrane of
presynaptic neurons When an AP reaches the terminal button,
voltage-activated Ca2+ channels open & Ca2+ rushes in◦ Ca2+ causes the vesicles to fuse with the
membrane & release contents into the synaptic cleft
Release of NTs
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NTs released from the presynaptic neuron cross the cleft & bind to receptors on the postsynaptic neuron
Receptors contain binding sites for only certain NTs
Any molecule that binds is a ligand There are often multiple receptors that
allow one kind of NT to bind: receptor subtypes◦ Different subtypes can cause different reactions
Activation of Receptors by NTs
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There are 2 general types of receptors1. Ionotropic
◦ NT binds & ion channel opens & ions flow through
◦ Immediate reaction
2. Metabotropic◦ NT binds & initiates a G-protein to trigger a
second messenger, which moves within the cell to create a reaction
◦ Slow, longer lasting effects◦ More abundant
Receptors
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A special type of metabotropic receptor Located on the presynaptic neuron & bind
with NTs from its own neuron Function to monitor the # of NTs in the
synapse◦ If too few, signal to release more◦ Too many, signal to slow/stop release
Autoreceptor
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In order to allow the synapses to be available to signal again, the extra NT in the synaptic cleft need to be “cleaned up” by:
Reuptake◦ Most of the extra NT are quickly taken back into the
presynaptic neuron by transporters to be repackaged in vesicles for future release
Enzymatic degradation◦ NTs in the cleft are broken down by enzymes◦ Ex: acetylcholine broken down by acetylcholinesterase◦ Even these pieces are taken back into the neuron &
recycled
Reuptake, Degradation & Recycling
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Unique signal transmission alternative to traditional synapses
Called electrical synapses Narrow gaps between neurons connected by
fine tubes called connexins that let electrical signals pass
Very fast & allow communication in both directions
Not yet fully understood in mammalian systems
Gap Junctions
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Amino Acid NTs Monoamine NTs Acetylecholine Unconventional/Misc. NTs Neuropeptides
Neurotransmitters
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AAs are the building blocks of proteins Glutamate
◦ Most common excitatory NT in the CNS Aspartate Glycine GABA
◦ Most common inhibitory NT
Amino Acid NTs
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2 groups with a total of 4 NTs in this class Catecholamines:1. Dopamine (DA)
◦ Made from tyrosine/L-Dopa
2. Norepinephrine (NE)◦ Made from dopamine
3. Epinephrine◦ Made from NE
Indolamines:4. Serotonin (5-HT)
◦ Made from tryptophan
Monoamines
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Functions at neuromuscular junctions, in ANS & CNS
Extra is mostly broken down in the synapse; by acetylcholinesterase
Receptors for Ach are said to be cholinergic
Acetylcholine (Ach)
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Act differently than traditional NTs Nitric oxide & carbon monoxide
◦ Gases that diffuse across the membrane, across the extracellular fluid & across the membrane of the next neuron
Endocannabinoids◦ Essentially, the brain’s natural version of THC
(main active chemical in marijuana)◦ Ex: annandimide
Unconventional/Misc. NTs
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Don’t worry about the specific types Just know that they are another type of NT Generally large NTs
Neuropeptides
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Pharmaceutical drugs generally affect synaptic in 2 ways◦ Agonists facilitate the effects of a NT
Can bind to a receptor & activate it like the NT would◦ Antagonists inhibit
Can bind to a receptor & block it so NTs cannot bind
Drugs & Synaptic Transmission
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Acetylcholine has 2 types of receptors1. Nicotinic
◦ Many in the PNS between motor neurons & muscle fibers
◦ Ionotropic◦ Nicotine: agonist◦ Curare: antagonist (causes paralysis)◦ Botox: antagonist
2. Muscarinic◦ Many located in the ANS◦ Metabotropic◦ Atropine: antagonist, receptor blocker
Example
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Endogenous◦ Compounds naturally made within the body◦ Ex: enkephalins & endorphins
The body’s endogenous opioids An exogenous opioid is morphine Opioids are analgesics (pain relievers)
Misc.