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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.
The neuromuscular junction is the synapse that is formed between an alpha motor neuron (α-MN) and the skeletal muscle fiber. In order for a muscle to contract, an action potential is first propagated down a nerve until it reaches the axon terminal of the motor neuron.
In some invertebrates, glutamate is the main excitatory transmitter at the neuromuscular junction. [3] [4] In the neuromuscular junction of vertebrates, EPP (end-plate potentials) are mediated by the neurotransmitter acetylcholine, which (along with glutamate) is one of the primary transmitters in the central nervous system of invertebrates. [5]
A special case of a chemical synapse is the neuromuscular junction, in which the axon of a motor neuron terminates on a muscle fiber. [ae] In such cases, the released neurotransmitter is acetylcholine, which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the sarcolemma) of the muscle fiber.
The neuromuscular junction (NMJ) is the most well-characterized synapse in that it provides a simple and accessible structure that allows for easy manipulation and observation. The synapse itself is composed of three cells: the motor neuron , the myofiber , and the Schwann cell .
One-leg stands — bend one knee to lift your foot ahead of you until the knee is aligned with the hips. Repeat a few times on each side and get assistance from a chair or wall if needed.
The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction.
Long-term potentiation (LTP) is one mechanism where repeated EPSPs occur, strengthening neural circuits involved in learning, allowing the brain to store information more effectively. Long-term depression (LTD) is another mechanism where IPSPs occur weakening less-used synapses, refining learning by filtering out unnecessary information.