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Lecture

Neuromuscular junction

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Department
Physiology
Course
Physiology 3120
Professor
Tom Stavraky
Semester
Fall

Description
Human Physiology Monday, October 5, 2009 Neuromuscular Junction • RMP in muscle cells is -90mV • Sequence of events in neuromuscular transmission 1. Action potential in alpha-motor nerve 2. Depolarization of alpha-motor nerve terminal 3. Voltage-gated calcium channels open 4. Influx of calcium 5. Movement of calcium causes fusing of ACh vesicles to membrane terminal, and releases ACh in quantal amounts 6. Diffusion of ACh to muscle cell membrane endplate 7. Attachment of ACh to nicotinic ACh receptors at endplate 8. Opening of non-specific cation channels (ligand-gated channels)  Increased conductance of both sodium & potassium  Preferential influx of sodium because RMP of muscle cell is at the equilibrium potential for potassium 9. Preferential influx of sodium into muscle cell 10. Depolarization of muscle cell membrane at the endplate (endplate potential [EPP])  no AP yet 11. Local currents open voltage-gated sodium & potassium channels on membrane adjacent to endplate  production of AP 12.AP propagates outward in all directions along muscle cell  Muscle cells not myelinated 13. ACh broken down to choline & acetate by acetylcholinesterase  The enzyme is found on the basement membrane • 1 AP in alpha-motor nerve = 1 AP in muscle cell membrane • Evidence for the action of ACh at the NMJ 1. EPP prolonged by inhibition of acetylcholinesterase (i.e. neostigmine)  Prevent ACh from breaking down; better chance of finding a receptor and gates stay open longer 2. EPPs are inhibited by ACh receptor competitors (i.e. succinylcholine) 3. Exogenous (external sources of) ACh causes EPPs 4.
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