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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 in this category include snake venom poisoning, botulism, arthropod poisoning, organophosphates and hypermagnesemia.(reference 13) Organophosphates are present in many insecticides and herbicides. They are also the basis of many nerve gases.(reference 27) Hypermagnesmia is a condition where the balance of ...
Neuromuscular disease can also be diagnosed by various blood tests and using electrodiagnostic medicine tests [23] including electromyography [24] (measuring electrical activity in muscles) and nerve conduction studies. [25] Genetic testing is an important part of diagnosing inherited neuromuscular conditions. [23]
Limb girdle muscular dystrophies (LGMD) as defined by the European Neuromuscular Centre in 2018. [1] [2] They are named by the following system: LGMD, recessive or dominant inheritance (R or D), order of discovery (number), affected protein. [1] LGMD D1 DNAJB6-related; LGMD D2 TNP03-related; LGMD D3 HNRNPDL-related; LGMD D4 calpain3-related
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 ]
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.
The electrical impulse travels along the pre-synaptic neurone axon to synapse with the muscle at the neuromuscular junction (NMJ) to cause muscle contraction. [17] When the action potential reaches the axon terminal, it triggers the opening of the calcium ion gated channels, which causes the influx of Ca 2+.
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]