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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 structure of the autonomic neuromuscular junction consists of several essential features including that: the terminal portions of autonomic nerve fibers are varicose and mobile, transmitters being released 'en passage' from varying distances from the effector cells; while there is no structural post-junctional specialization on effector ...
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 .
MuSK (for Muscle-Specific Kinase) [1] is a receptor tyrosine kinase required for the formation and maintenance of the neuromuscular junction. [2] It is activated by a nerve-derived proteoglycan called agrin , [ 3 ] which is similarly also required for neuromuscular junction formation.
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.
Perisynaptic schwann cells (also known as Terminal schwann cells or Teloglia) are neuroglia found at the Neuromuscular junction (NMJ) with known functions in synaptic transmission, synaptogenesis, and nerve regeneration. [1] These cells share a common ancestor with both Myelinating and Non-Myelinating Schwann Cells called Neural Crest cells.
Nerve conduction studies can only diagnose diseases on the muscular and nerve level. They cannot detect disease in the spinal cord or the brain. In most disorders of the muscle, nerve, or neuromuscular junction, the latency time is increased. [12] This is a result of decreased nerve conduction or electrical stimulation at the site of the muscle.
Several motorneurons compete for each neuromuscular junction, but only one survives until adulthood. [36] Competition in vitro has been shown to involve a limited neurotrophic substance that is released, or that neural activity infers advantage to strong post-synaptic connections by giving resistance to a toxin also released upon nerve stimulation.