Linked Life Data

1977887

Source:http://linkedlifedata.com/resource/pubmed/id/1977887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1990-12-20
pubmed:abstractText
alpha-Latrotoxin causes a massive release of endogenous glutamate from guinea-pig cerebrocortical synaptosomes. There appear to be two components to the release. In the first 2 min following addition of 1.3 nM alpha-latrotoxin, glutamate release is largely energy dependent. Superimposed upon this release is a more slowly developing but ultimately much more extensive release of cytoplasmic glutamate together with gamma-aminobutyric acid and nonvesicular amino acids such as aspartate and alpha-aminoisobutyrate. In parallel with this cytoplasmic release there is an extensive depletion of ATP, a massive rise in cytoplasmic free Ca2+ concentration, and a severe restriction of synaptosomal respiratory capacity. The cytoplasmic release is only partially Na+ dependent, eliminating a simple reversal of the plasma membrane acidic amino acid carrier. It is concluded that alpha-latrotoxin releases both transmitter and cytoplasmic pools of amino acids in synaptosomes and causes a major disruption of terminal integrity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2039-47
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Alpha-latrotoxin releases both vesicular and cytoplasmic glutamate from isolated nerve terminals.
pubmed:affiliation
Department of Biochemistry, University of Dundee, Scotland.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't