1. 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

2. Physiological Anatomy of the Neuromuscular Junction
Motor End Plate
Fig. 7.1

3. Secretion of Acetylcholine by the Nerve Terminals
Fig. 7.2

4. Effects of Acetylcholine (AcH)
On the inside surface of the neural membrane are linear “dense” bars
Voltage gated channels lie to each side of the dense bars
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
Fig. 7.2 shows many acetylcholine receptors in the membrane
Two molecules of AcH must attach to the receptor
The channels open and allow Na+, Ca+, or K+ ions to move through
easily; but not negative ions such as Cl-
Far more Na+ ions pass through for two reasons (1) there are only
two 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

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

6. Acetylcholine (cont.)
Destruction of the Released Acetylcholine
Most of the AcH is destroyed by the enzyme
acetylcholinesterase
A small amount diffuses out of the synaptic
space
The few milliseconds it remains is enough
to excite the muscle fiber

7. Acetylcholine (cont.)
End Plate Potential and Excitation of the Muscle
The sudden influx of Na+ ions causes the electrical
potential to increase in the positive direction as
much as mV
This creates a local potential called the End Plate
Potential

8. End Plate Potentials
Fig 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:

9. Fatigue of the Junction
Safety factor for transmission at the neuromuscular
junction
Each impulse that arrives at the junction causes about
3X as much end plate potential as required to stimulate
the muscle
The stimulation, however, diminishes the number of
AcH vesicles
Fatigue of the junction occurs rarely and only then if
at exhausting levels of muscle activity

10. Muscle Action Potential
Skeletal Muscle
Large Nerves
Resting Membrane Potential
-80 to -90 mV
Duration of the
Action Potential
1-5 milliseconds
milliseconds
Velocity of Conduction
3-5 m/sec
39-65 m/sec

11. Spread of the AP via Transverse Tubules
Muscle AP (cont.)
Spread of the AP via Transverse Tubules
Fig Transverse (T) tubule-
sarcoplamic reticulum system

12. Excitation-Contraction Coupling
T-Tubule-Sarcoplasmic Reticulum System (Triads)
T-tubules are small and run transverse to the myo-
fibrils
They penetrate all the way from one side of the
muscle cell to the other side
Where the T-tubules originate from the cell
membrane, they are open to the exterior of the fiber
They are actually internal extensions of the
cell membrane
The sarcoplasmic reticulumis composed of 2 parts:
(1) large chambers called termnal cisternae
(2) long longitudinal tubules

13. Excitation-Contraction Coupling (cont.)
Release of Calcium Ions by the Sarcoplasmic Reticulum
As the AP reaches the T-tubule, the voltage change
is sensed by dihydropyridine receptors linked to calcium
release channels, also called ryanodine receptors
b. Triggers the release of Ca++ initiating contraction

14. Fig. 7.6 Excitation-coupling in skeletal
muscle.

15. Fig 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.

16. Excitation-Contraction Coupling (cont.)
Calcium pump removes calcium ions after
contraction occurs-binds calcium to calsequestrin