Linked Life Data

8065451

Source:http://linkedlifedata.com/resource/pubmed/id/8065451

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6491
pubmed:dateCreated
1994-9-16
pubmed:abstractText
During synaptic transmission in the nervous system, synaptic vesicles fuse with the plasma membrane of presynaptic terminals, releasing neurotransmitter by exocytosis. The vesicle membrane is then retrieved by endocytosis and recycled into new transmitter-containing vesicles. Exocytosis in synaptic terminals is calcium-dependent, and we now report that endocytosis also is regulated by the intracellular calcium concentration ([Ca2+]i). Capacitance measurements in synaptic terminals of retinal bipolar neurons revealed that endocytosis was strongly inhibited by elevated [Ca2+]i in the range achieved by Ca(2+)-current activation. The rate of membrane retrieval was steeply dependent on [Ca2+]i, with a Hill coefficient of 4 and half-inhibition at approximately 500 nM. At [Ca2+]i > or = 900 nM, endocytosis was entirely absent. The action of internal calcium on endocytosis represents a novel negative-feedback mechanism controlling the rate of membrane recovery in synaptic terminals after neurotransmitter secretion. As membrane retrieval is the first step in vesicle recycling, this mechanism may contribute to activity-dependent synaptic depression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
370
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
652-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Inhibition of endocytosis by elevated internal calcium in a synaptic terminal.
pubmed:affiliation
Department of Neurobiology and Behavior, State University of New York, Stony Brook, 11794-5230.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.