Linked Life Data

9252190

Source:http://linkedlifedata.com/resource/pubmed/id/9252190

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6642
pubmed:dateCreated
1997-8-27
pubmed:abstractText
Repetitive activation of excitatory synapses in the central nervous system results in a long-lasting increase in synaptic transmission called long-term potentiation (LTP). It is generally believed that this synaptic plasticity may underlie certain forms of learning and memory. LTP at most synapses involves the activation of the NMDA (N-methyl-D-aspartate) subtype of glutamate receptor, but LTP at hippocampal mossy fibre synapses is independent of NMDA receptors and has a component that is induced and expressed presynaptically. It appears to be triggered by a rise in presynaptic Ca2+, and requires the activation of protein kinase A, which leads to an increased release of glutamate. A great deal is known about the biochemical steps involved in the vesicular release of transmitter, but none of these steps has been directly implicated in long-term synaptic plasticity. Here we show that, although a variety of short-term plasticities are normal, LTP at mossy fibre synapses is abolished in mice lacking the synaptic vesicle protein Rab3A.
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
7
pubmed:volume
388
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
590-3
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Rab3A is essential for mossy fibre long-term potentiation in the hippocampus.
pubmed:affiliation
Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't