FIGURE 19 Summary diagram of the membrane channels important for the process of synaptic transmission at the skeletal neuromuscular junction. Dep, depolarization.
to the high resting K+ permeability. At rest, a small amount of transmitter release occurs because of the spontaneous release of vesicles (quanta) from the presynaptic terminal. The spontaneous release is presumably due to the low basal levels of Ca2+ in the presynaptic terminal. The resultant MEPPs are only approximately 0.4 mV and are insufficient to trigger an action potential in the muscle cell. When an action potential propagates down the motor axon, it eventually invades the presynaptic terminal. As the action potential invades the terminal, the terminal is depolarized, and that depolarization leads to the opening of voltage-dependent Ca2+ channels. Calcium ions move down their electrochemical gradient and enter the terminal. The resultant increase in the intracellular Ca2+ concentration leads to the release of 100 or so synaptic vesicles, each containing 104 molecules of ACh. The released ACh diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. The binding of ACh with ACh-sensitive channels causes individual channels that are normally closed to open in an all-or-nothing fashion. The chemically gated channels opened
TABLE 1 Properties of Action Potentials and Synaptic Potentials at the Skeletal Neuromuscular Junction
Synaptic potential (End-plate potential)
Changes in membrane conductance Duration, rising phase (initiation) Duration, falling phase
Equilibrium potential Pharmacology
Propagation Other features
Initiated by ACh
Simultaneous chemically gated increase in gNa and gk Passive decay; diffusion and acetylcholinesterase (AChE) 10-20 msec
Reversal potential close to 0 mV Blocked by curare; enhanced by neostigmine;
not blocked by tetrodotoxin (TTX) Propagates with decrement No evidence for regenerative action or refractory period
Initiated by depolarization (the end-plate potential) Specific voltage-dependent increase in gNa
Specific increase in gk and decrease in gNa
Blocked by TTX but not by curare;
not affected by neostigmine All-or-nothing
Regenerative rise, followed by absolute and relative refractory periods by ACh are distinct from the voltage-gated channels (Na+ and K+) that underlie the action potential in the axon and skeletal muscle cell. The channel opened by ACh is equally permeable to Na+ and K+, and as a result the postsynaptic membrane is depolarized. This postsynaptic potential (the EPP), if sufficiently large (as it normally is), brings the muscle membrane potential to threshold. A new potential, the action potential, is initiated in the muscle cell by the voltage-dependent changes in Na+ and K+ permeabilities. The muscle action potential propagates along the muscle cell membrane and leads, by a process known as excitation-concentration coupling, to the development of muscle tension.
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