Linked Life Data

10678752

Source:http://linkedlifedata.com/resource/pubmed/id/10678752

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-3-9
pubmed:abstractText
Prior evidence indicates that synaptically-released zinc enters postsynaptic neurons in toxic excess during ischemia and seizures. In addition, prevention of this zinc translocation has been shown to be neuroprotective in both ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mechanical injury to the brain. Specifically, using a rat model of traumatic brain injury, we show that trauma is associated with (i) loss of zinc from presynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) neuroprotection by intraventricular administration of a zinc chelator just prior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
852
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
268-73
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury.
pubmed:affiliation
Center for Biomedical Engineering, UTMB, Galveston, TX 77555, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't