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Genomic and proteomic profiling reveals reduced mitochondrial function and disruption of the neuromuscular junction driving rat sarcopenia.
Activation of the neuromuscular junction will produce a synchronized contraction in the homonymous (target) muscle.
2001) previously found that GABA had both a presynaptic (increased transmitter release) and a postsynaptic (reduced muscle input resistance) action at the neuromuscular junction of several stomatogastric muscles in the lobster Homarus americanus.
Succinylcholine is resistant to the effects of acetylcholinesterase which allows a persistent and longer duration at the neuromuscular junction.
Myasthenia gravis is an autoimmune disorder mainly caused by antibodies to the nicotinic acetylcholine receptors (AChR) of the neuromuscular junction [1].
Topics include cell adhesion molecules at the Drosophilia neuromuscular junction, synapse formation in the mammalian central nervous system, developmental axonal pruning and synaptic plasticity, cell adhesion molecules in synatopathies, the cadherin superfamily in synapse formation and function, nectins and nectin-like molecules in the nervous system, the Down syndrome cell adhesion molecule, molecular basis of lamina-specific synaptic connections in the retina, cell adhesion molecules of the NCAM family and their roles at synapses, ephrins and eph receptor tyrosine kinases in synapse formation, the role of integrins at synapses, and extracellular matrix molecules in neuromuscular junctions and central nervous system synapses.
Botulinum neurotoxins (BoNTs) primarily act at the neuromuscular junction by decreasing the release of acetylcholine and causing a blockade effect at the neuromuscular junction between nerves and muscle (Cherington, 2004).
Quantal transmitter telease at botulinum-treated vertebrate neuromuscular junction.
More than 85% of MG patients have antibodies to the acetylcholine receptor (AChR) at the neuromuscular junction or are seropositive for MG (SPMG).
Myasthenia Gravis (MG) is the best understood of the various autoimmune diseases and affects the neuromuscular junction postsynaptically.
A light and transmission electron microscopy study was performed in skeletal muscles (SM) Gastrocnemius (G) from mice experimentally infected with Trypanosoma cruzi to determine changes on microvessels (MV) and neuromuscular junction (NMJ) of G.

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