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Repetitive nerve stimulation (RNS) was originally widely applied in the functional evaluation of neuromuscular junctions (NMJs), where it became a routine examination of the NMJ diseases such as myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome. Since the first description by Mulder et al .
Evaluation of the NMJs. For the study of the NMJs, the proximal part of the left antimere of the EDL muscle was removed and immersed in Karnovsky at room temperature.
Within 1-2 days, the MNs projected axons, and after more than 1 week in culture, the MNs formed NMJs with the muscle cells.
A subsequent study further determined that the 14-3-3[zeta] protein progressively accumulates to the synaptic boutons during maturation of the neuromuscular junction (NMJ), where it colocalizes with the synaptic vesicles containing the neurotransmitter glutamate .
(1) Aging-induced neuromuscular junction (NMJ) remodeling entails reductions in the number of presynaptic vesicles, nerve terminals, and nicotinic acetylcholine receptors (nAChRs) together with an increase in the space at the motor end plate.
Abbreviations: PNS: peripheral nervous system; NMJ: neuromuscular junction; CNS: central nervous system; EM: electron microscopy; FIB-SEM: focused ion beam/scanning electron microscopy; GFP: green fluorescent protein; PSD: postsynaptic density; NMDA: N-methyl-D-aspartic acid; AMPA: a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; TARP: transmembrane AMPA receptor regulatory protein; ASD: autism spectrum disorder; CNV: copy number variation; IEG: immediately early gene; FRAP: fluorescence recovery after photobleaching; GKAP: guanylate kinase-associated protein; LRRTM: leucinerich repeat transmembrane protein; SALM: synaptic adhesion-like molecule; YFP: yellow fluorescent protein; CFP: cyan fluorescent protein.
botulinum, A, B, [C.sub.1], [C.sub.2], D, E, F, and G, all of which interfere with neural transmission by blocking the release of acetylcholine at the neuromuscular junction (NMJ) and reduce muscle activity.
The detrimental role of TNFR2 was confirmed in vivo in [SOD1.sup.G93A] mice knockout for the receptor, where there was a partial but significant protection of motor neurons in the lumbar spinal cord and spared neuromuscular junctions (NMJ) and conserved morphology of tibialis muscle fibers .
As all of the gross physiological components to perform the corkscrew-roll appear to be in place in first- and second-instar animals, we speculate that maturation of the NMJ may be required for the corkscrew-roll nocifensive response in the third-instar larvae.
Notably, neuron-type specificity at muscle 4 NMJ compared to muscle 6 and 7 NMJs regarding Drosophila neurotrophic was observed .
Two slides from each animal were used for the morphometric study of the NMJs. In each studied animal, the area and the major and minor diameter of 50 were determined.
Myasthenia gravis (MG) is an autoimmune disease that affect the neuromuscular junction (NMJ) in which most antibodies are directed against the acetylcholinesterase receptor (AChR).
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