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Vogel, K. Sneyders de; Zumthor, Paul; S., J. H.; S., J.; Stockum, Th. C. van; Janssen, H. H.

doi:10.1007/bf01515085

Cited by 2 publications

(2 citation statements)

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“…T h e kinetic changes induced by NSF peptides might result from slowi~lg of a reaction that causes each synaptic vesicle to fuse [for example, dilation of a fusion pore (3 1 )] or from desy~lchro~liza-tion of i~ldividual vesicle filsio~l events (32). Desynchronizatio~l of vesicle f u s i o~~ could result from a reduction in the number of fusogenic particles per vesicle, with inhibition occurring when the number of particles has been reduced to zero (33). Incorporating such temporal control into the basic mechanism of tnembrane fusion provides an economical means of defining the rate of synaptic transmission and, thereby, the integrative properties of synapses (34).…”

Section: Mg2+ Bindingmentioning

confidence: 99%

Regulation of Neurotransmitter Release Kinetics by NSF

Schweizer

Dresbach

DeBello

et al. 1998

Science

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NSF (N-ethylmaleimide-sensitive factor) is an adenosine triphosphatase (ATPase) that contributes to a protein complex essential for membrane fusion. The synaptic function of this protein was investigated by injecting, into the giant presynaptic terminal of squid, peptides that inhibit the ATPase activity of NSF stimulated by the soluble NSF attachment protein (SNAP). These peptides reduced the amount and slowed the kinetics of neurotransmitter release as a result of actions that required vesicle turnover and occurred at a step subsequent to vesicle docking. These results define NSF as an essential participant in synaptic vesicle exocytosis that regulates the kinetics of neurotransmitter release and, thereby, the integrative properties of synapses.

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Section: Mg2+ Bindingmentioning

confidence: 99%

Regulation of Neurotransmitter Release Kinetics by NSF

Schweizer

Dresbach

DeBello

et al. 1998

Science

View full text Add to dashboard Cite

show abstract

“…In rats (46), mice (64), and goldfish (53), exposed experimentally to cupric ion in toxic amounts, copper has been visualized histochemically in associa tion with histologic degeneration principally in tubular epithelium. Copper and necrosis have also been seen in'the cytoplasm of renal tubular epithelium of five patients dying of Wilson's disease (65), and the pathologic renal physiology seen in the illness is chiefly, though not wholly, tubular (66).…”

Section: Pathogenesis and Copper Metabolismmentioning

confidence: 99%