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[10] P. Paul, J de Belleroche, The role of D-amino acids in
[10] P. Paul, J de Belleroche, The role of D-amino acids in

... obtained which exhibited marked effects on motor phenotype. At 8 months, abnormal ...
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... their individual dynamics. This is true also for small nerve systems such as central r h y t h m generators [6, 7] and cerebral cortex neurons [8, 9] where the role of separate elements of an ensemble is played by structures consisting of a large number of neurons connected by an "all with each" fea ...
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Neuromuscular junction



A neuromuscular junction (sometimes called a myoneural junction) is a junction between nerve and muscle; it is a chemical synapse formed by the contact between the presynaptic terminal of a motor neuron and the postsynaptic membrane of a muscle fiber. It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction.Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) 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 Duchenne muscular dystrophy, 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.
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