Linked Life Data

12373554

Source:http://linkedlifedata.com/resource/pubmed/id/12373554

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2002-10-9
pubmed:abstractText
The fungal toxin cytochalasin D as well as endogenous gelsolin depolymerize filamentous actin which may induce dynamic uncoupling of membrane ion channels. In vitro application of cytochalasin D reduced NMDA-induced [(3)H]noradrenaline release from mouse brain neocortical slices by 38%. In gsn deficient neocortical synaptosomes [Ca(2+)](i) increase in response to K(+) (30 mM) depolarization was 33% higher than in wild-type. After transient focal cerebral ischemia K(+)-induced [Ca(2+)](i) increase in neocortical synaptosomes was 56% lower than in synaptosomes prepared from the non-ischemic contralateral hemisphere. After in vivo pretreatment with cytochalasin D 10 min before MCA occlusion K(+)-induced [Ca(2+)](i) increase in synaptosomes in vitro prepared 1 h after reperfusion from the ischemic hemisphere was only 25% lower than in contralateral synaptosomes, while cytochalasin D pretreatment in vivo did not reduce K(+)-induced [Ca(2+)](i) increase in vitro. Hence, presynaptic Ca(2+) influx and subsequently neuronal vulnerability are attenuated by increased and are aggravated by decreased F-actin depolymerization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0939-4451
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
325-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Effects of cytoskeletal modifications on Ca2+ influx after cerebral ischemia.
pubmed:affiliation
Department of Pharmacology, University of Bonn, Bonn, Germany. finkk@uni-bonn.de
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't