| Neuromuscular junction | |
|---|---|
 At the neuromuscular junction, the nerve fiber is able to transmit a signal to the muscle fiber by releasing ACh (and other substances), causing muscle contraction | |
 Schematic view of a neuromuscular junction | |
| Details | |
| Identifiers | |
| Latin | synapssis neuromuscularis; junctio neuromuscularis |
| MeSH | D009469 |
| TH | H2.00.06.1.02001 |
| FMA | 61803 |
| Anatomical terminology | |
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A neuromuscular junction (or myoneural junction) is a chemical synapse between a motor neuron and a muscle fiber.[1]
It allows the motor neuron to transmit a signal to the muscle fiber, causing muscle contraction.[2]
Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. In the neuromuscular system, nerves from the central nervous system and the peripheral nervous system are linked and work together with muscles.[3] Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-gated calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmins) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Congenital myasthenic syndrome, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
- ^ Levitan I, Kaczmarek L (August 19, 2015). "Intercellular communication". The Neuron: Cell and Molecular Biology (4th ed.). New York, NY: Oxford University Press. pp. 153–328. ISBN 978-0199773893.
- ^ Jimsheleishvili S, Marwaha K, Sherman AL (2024), "Physiology, Neuromuscular Transmission", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 31082177, retrieved 2024-08-26
- ^ Rygiel KA, Picard M, Turnbull DM (August 2016). "The ageing neuromuscular system and sarcopenia: a mitochondrial perspective". The Journal of Physiology. 594 (16): 4499–4512. doi:10.1113/JP271212. PMC 4983621. PMID 26921061.