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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 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]
In biology, a motor unit is made up of a motor neuron and all of the skeletal muscle fibers innervated by the neuron's axon terminals, including the neuromuscular junctions between the neuron and the fibres. [1] Groups of motor units often work together as a motor pool to coordinate the contractions of a single muscle.
The neuromuscular junction diseases present within this subset are myasthenia gravis, and Lambert-Eaton syndrome.(reference 26) In each of these diseases, a receptor or other protein essential to normal function of the junction is targeted by antibodies in an autoimmune attack by the body. [citation needed]
A neuroeffector junction is a site where a motor neuron releases a neurotransmitter to affect a target—non-neuronal—cell. This junction functions like a synapse . However, unlike most neurons, somatic efferent motor neurons innervate skeletal muscle, and are always excitatory.
Myasthenia gravis is an autoimmune disease of the neuromuscular junction which results from antibodies that block or destroy nicotinic acetylcholine receptors (AChR) at the junction between the nerve and muscle. [6] [7] [1] This prevents nerve impulses from triggering muscle contractions. [1]
In myasthenia gravis, the receptor at the neuromuscular junction is targeted by antibodies, leading to muscle weakness. Muscarinic acetylcholine receptors can be blocked by the drugs atropine and scopolamine. Congenital myasthenic syndrome (CMS) is an inherited neuromuscular disorder caused by defects of several types at the neuromuscular ...
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 ...