Unit Two: Membrane Physiology, Nerve, and

Muscle

Chapter 7: Excitation of Skeletal Muscle: Neuromuscular Transmission and

Excitation-Coupling

Guyton and Hall, Textbook of Medical Physiology, 12th edition

Physiological Anatomy of the Neuromuscular Junction

• Motor End Plate

Fig. 7.1

Fig. 7.2

• Secretion of Acetylcholine by the Nerve Terminals

a. On the inside surface of the neural membrane are linear “dense” bars

b. Voltage gated channels lie to each side of the dense bars

c. When an AP spreads over the terminal end, the channels open and Ca++ exerts an influence of the acetylcholine vesicles and it is released into the synaptic space

• Effect of Acetylcholine on the Postsynaptic Muscle Membrane

a. Fig. 7.2 shows many acetylcholine receptors in the membrane

b. Two molecules of AcH must attach to the receptorc. The channels open and allow Na+, Ca+, or K+ ions to

move througheasily; but not negative ions such as Cl-

d. Far more Na+ ions pass through for two reasons (1) there are onlytwo positive ions in great concentration (Na +outside and K+ inside)and (2) the negative potential on the inside pulls the Na+ in and prevents the K+ from passing outside the cell

Effects of Acetylcholine (AcH)

Fig. 7.3 Acetylcholine gated channels A. Closed B. After AcH attaches

Acetylcholine (cont.)

• Destruction of the Released Acetylcholine

a. Most of the AcH is destroyed by the enzymeacetylcholinesterase

b. A small amount diffuses out of the synapticspace

c. The few milliseconds it remains is enoughto excite the muscle fiber

Acetylcholine (cont.)

• End Plate Potential and Excitation of the Muscle

a. The sudden influx of Na+ ions causes the electricalpotential to increase in the positive direction asmuch as 50-75 mV

b. This creates a local potential called the End PlatePotential

End Plate Potentials

Fig. 7.4 End Plate Potentials in mV. A: weakened end potential in a muscle too weak to elicit an AP; B: Normal end plate potential eliciting an AP; C:

• Fatigue of the Junction

a. Safety factor for transmission at the neuromuscularjunction

b. Each impulse that arrives at the junction causes about3X as much end plate potential as required to stimulatethe muscle

c. The stimulation, however, diminishes the number ofAcH vesicles

d. Fatigue of the junction occurs rarely and only then ifat exhausting levels of muscle activity

Muscle Action Potential

Skeletal Muscle

Large Nerves

Resting Membrane Potential

-80 to -90 mV -80 to -90 mV

Duration of theAction Potential

1-5 milliseconds .2-1.0 milliseconds

Velocity of Conduction 3-5 m/sec 39-65 m/sec

Muscle AP (cont.)

• Spread of the AP via Transverse Tubules

Fig. 7.5 Transverse (T) tubule- sarcoplamic reticulum system

Excitation-Contraction Coupling

• T-Tubule-Sarcoplasmic Reticulum System (Triads)

a. T-tubules are small and run transverse to the myo-fibrils

b. They penetrate all the way from one side of the muscle cell to the other side

c. Where the T-tubules originate from the cell membrane, they are open to the exterior of the fiber

d. They are actually internal extensions of the cell membrane

e. The sarcoplasmic reticulumis composed of 2 parts:(1) large chambers called termnal cisternae(2) long longitudinal tubules

Excitation-Contraction Coupling (cont.)

• Release of Calcium Ions by the Sarcoplasmic Reticulum

a. As the AP reaches the T-tubule, the voltage change is sensed by dihydropyridine receptors linked to calciumrelease channels, also called ryanodine receptors

b. Triggers the release of Ca++ initiating contraction

Fig. 7.6 Excitation-coupling in skeletal muscle.

Fig. 7.7 Excitation-contraction coupling in the muscle showing (1) an AP that causes the release of Ca ions from the sarcoplasmic reticulum and then (2) re-uptake of the calcium ions by the calcium pump.

Excitation-Contraction Coupling (cont.)

• Calcium pump removes calcium ions after contraction occurs-binds calcium to calsequestrin