Synapses are found across the body, typically at the connection point between neurons. One of the most heavily-studied synapse is at the neuromuscular junction (NMJ). The NMJ is a synapse that connects a motor neuron with the muscle fiber. Most skeletal muscle movements in the body are controlled by neurotransmitter release from a motor neuron into the NMJ. The mechanism by which this occurs is described step-by-step below:
1. An action potential arrives at the axon terminal of the motor neuron, opening Ca2+ channels.
2. The influx of Ca2+ causes vesicles containing acetylcholine (ACh), a neurotransmitter, in the axon terminal to fuse with the plasma membrane, releasing the chemical into the synapse. This is called exocytosis.
3. ACh diffuses across the synapse and binds to nicotinic receptors – ligand-gated ion channels in the muscle fiber plasma membrane. The ion channels open and lead to contractions in the muscle fiber.
4. Acetylcholinesterase (AChE) present in the synapse rapidly degrades any remaining ACh into choline and acetate.
5. Choline is reabsorbed back into the presynaptic cell by endocytosis to be recycled.
Different conditions exist that have their effect at several of these steps. Some are listed below:
|Lambert-Eaton myasthenic syndrome (LEMS)||Destruction of pre-synaptic Ca2+ channels|
|Congenital AChE deficiency||Lack of AChE|
|Myasthenia gravis||Destruction of post-synaptic nicotinic ACh receptors|
Acetylcholinesterase also exists in the synapses of muscarinic ACh receptors, which are the receptors of the parasympathetic nervous system (PNS). The PNS is involved in “”rest and digest”” functions, including dilation of blood vessels, slowing of heart rate, pupil constriction, and activation of gastrointestinal system.
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