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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.
Neuromuscular junction diseases are a result of a malfunction in one or more steps of the above pathway. As a result, normal functioning can be completely or partially inhibited, with the symptoms largely presenting themselves as problems in mobility and muscle contraction as expected from disorders in motor end plates.
Muscles contract when they receive signals from motor neurons. The neuromuscular junction is the site of the signal exchange. The steps of this process in vertebrates occur as follows: (1) The action potential reaches the axon terminal. (2) Calcium ions flow into the axon terminal. (3) Acetylcholine is released into the synaptic cleft. (4 ...
Much of our understanding of synapse formation comes from studies at the neuromuscular junction. The transmitter at this synapse is acetylcholine. The acetylcholine receptor (AchR) is present at the surface of muscle cells before synapse formation. The arrival of the nerve induces clustering of the receptors at the synapse.
In the muscle-type receptors, found at the neuromuscular junction, receptors are either the embryonic form, composed of α 1, β 1, γ, and δ subunits in a 2:1:1:1 ratio ((α 1) 2 β 1 γδ), or the adult form composed of α 1, β 1, δ, and ε subunits in a 2:1:1:1 ratio ((α 1) 2 β 1 δε).
Note the differences in the scales on the X- and Y-axes. Both are taken from recordings at the mouse neuromuscular junction. End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called "end plates ...
During the 1950s, Bernard Katz and Paul Fatt observed spontaneous miniature synaptic currents at the frog neuromuscular junction. [33] Based on these observations, they developed the 'quantal hypothesis' that is the basis for our current understanding of neurotransmitter release as exocytosis and for which Katz received the Nobel Prize in ...
Depolarizing neuromuscular blockers: Depolarizing neuromuscular blockers directly bind to postsynaptic cholinergic receptors of the neuromuscular junction to generate a sustained action potential. This causes prolonged stimulation and desensitization of neuroreceptors, causing skeletal muscle relaxation effects such as paralysis. [ 1 ]