Skeletal muscle changes neuromuscular junction

The nicotinic acetylcholine (ACh) receptor is a well-characterized receptor of this type consisting of five subunits. It is present on the skeletal muscle cell end-plate in the neuromuscular junction, at all autonomic ganglia, and in the central nervous system (CNS). The function of this receptor is to convert ACh binding into an electrical signal via increased Na+ or K+ permeability across the cell membrane (i.e., membrane depolarization). When two molecules of ACh bind to the a subunit of the receptor, a conformational change in the receptor induces opening of the channel to at least 0.65 nm for approximately 1-2 ms. 

Skeletal muscles are controlled by large nerves in the spinal cord. The nerve cell or neuron is part of the spinal cord, but its projections, the axon and the many dendrites course outward to connect to muscle cells. The nerve axon is a sensory device that senses the muscle cells current condition. The dendrites are motor fibers that deliver the instructions to change its state to the muscle fiber. The area at which the muscle and nerve connect is called the neuromuscular junction. It is here that the end releases a chemical called a neurotransmit-ter that crosses the microscopic space between the nerve and muscle and causes the desired response. Five such neurotransmitters have been described acetylcholine, serotonin, norepinephrine, glycine, and gamma-ammi-nobutyric acid or GABA. Of these, the functions of three are known. Acetylcholine excites muscle activity and glycine and GABA inhibit it. 

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