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Publication : Alterations in transmission, vesicle dynamics, and transmitter release machinery at NCAM-deficient neuromuscular junctions.

First Author  Polo-Parada L Year  2001
Journal  Neuron Volume  32
Issue  5 Pages  815-28
PubMed ID  11738028 Mgi Jnum  J:73253
Mgi Id  MGI:2154808 Doi  10.1016/s0896-6273(01)00521-9
Citation  Polo-Parada L, et al. (2001) Alterations in Transmission, Vesicle Dynamics, and Transmitter Release Machinery at NCAM-Deficient Neuromuscular Junctions. Neuron 32(5):815-28
abstractText  Although functional neuromuscular junctions (NMJs) form in NCAM-deficient mice, they exhibit multiple alterations in presynaptic organization and function. Profound depression and unusual periodic total transmission failures with repetitive stimulation point to a defect in vesicle mobilization/cycling, and these defects were mimicked in (+/+) NMJs by inhibitors of myosin light chain kinase, known to affect vesicle mobilization. Two separate release mechanisms, utilizing different endocytic machinery and Ca(2+) channels, were shown to coexist in (-/-) terminals, with the mature process targeted to presynaptic membrane opposed to muscle, and an abnormally retained immature process targeted to the remainder of the presynaptic terminal and axon. Thus, NCAM plays a critical and heretofore unsuspected role in the molecular organization of the presynaptic NMJ.
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