Linked Life Data

8326831

Source:http://linkedlifedata.com/resource/pubmed/id/8326831

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-8-12
pubmed:abstractText
Neurons undergoing delayed neuronal death produced by hypoxia-ischaemia (HI) or status epilepticus (SE) showed a massive expression of c-Jun in their nuclei 24 h after the insult. With SE there was also a weaker induction of c-Fos and Jun B in dying neurons. SE induced in the presence of the NMDA antagonist MK-801 produced no delayed c-Jun expression in the hippocampus and nerve cell death did not occur in this region, although there was a delayed c-jun expression in the amygdala/piriform region, and cell death occurred in this area. Activation of central muscarinic receptors with pilocarpine, or block of D2 dopamine receptors with haloperidol, treatments which do not cause neuronal damage, strongly induced Fos and Jun B in hippocampal and striatal neurons, but only induced c-Jun very weakly. Thus, c-Jun may participate in the genetic cascade of events that produce programmed cell death in neurons.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0169-328X
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:geneSymbol
c-fos, c-jun, jun B
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
347-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Is c-Jun involved in nerve cell death following status epilepticus and hypoxic-ischaemic brain injury?
pubmed:affiliation
Department of Pharmacology, School of Medicine, University of Auckland, New Zealand.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't