NM transmission: Ions
Clinical - Neuromuscular Diseases and Disorders
The neuromuscular junction (NMJ) is the synapse (junction) between the axon terminal of a motor neuron and the motor end-plate. The motor end-plate is the excitable portion of the muscle cell membrane responsible for initiating the action potential (the cascade of ion shift which produces the electrical current across the cell and ultimately muscle contraction).
Neuromuscular communication is achieved primarily by neurotransmitters (NT) and in the influx/efflux of ions. The basic steps or this process are as follows:
- Action potential arrives at the terminal portion of the axon, which causes a conformational change in voltage gated Calcium channels allowing Calcium ions (Ca++) to flow into the neuron (at the terminal portion of the axon) from the extracellular fluid.
- Ca ions cause NT containing vesicles to fuse to the neuron’s cell membrane at the axon terminal. This fusion causes exocytosis and release of the vesicles’ NT (acetylcholine) into the synaptic cleft.
- Acetylcholine diffuses across the cleft and binds to nicotinic acetylcholine receptors.
- Binding of the receptors cause sodium ions (Na+) to enter the muscle cell and potassium ions (K+) to exit the cell; this process causes a local depolarization of the muscle cell = end plate potential (EPP).
- The depolarization spreads across the surface of the muscle fiber leading to a cascade of other ions ultimately leading to muscle contraction.
It is worth noting that the Na/K influx/efflux is very similar to the typical neuron action potential.