Linked Life Data

20977896

Source:http://linkedlifedata.com/resource/pubmed/id/20977896

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2011-1-3
pubmed:abstractText
Status epilepticus-induced hippocampal neuronal loss is mainly associated with excitotoxicity induced by increased levels of extracellular glutamate which is normally neutralized by high-affinity uptake mechanism. The energy source for the glutamate uptake is the electrochemical Na(+) gradient maintained by Na(+)/K(+) ATPase pump. In this study, we investigated the effect of early-life-induced status epilepticus on hippocampal Na(+)/K(+) ATPase activity and glutamate uptake. Rat pups 15 days old were injected i.p. with LiCl (3 mEq/kg) 12-18 h prior to s.c. pilocarpine administration (60 mg/kg). Hippocampal Na(+)/K(+) ATPase activity and glutamate uptake were evaluated 1.5, 12 and 24 h after SE induction. LiCl-pilocarpine-induced SE decreased Na(+)/K(+) ATPase activity and glutamate uptake by 42 and 38%, respectively, 1.5 h after SE induction. However, 12 and 24 h after SE induction the pump activity and glutamate uptake returned to control levels. SE early in life increased hippocampal number of degenerating neurons in the CA1 subfield and dentate gyrus 24 h after SE induction. In conclusion, SE induced early in life causes short-term disruption in hippocampal Na(+)/K(+) ATPase activity and glutamate uptake, which may be related to neuronal death found in CA1 subfield.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1872-6240
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
1369
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
167-72
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Early life LiCl-pilocarpine-induced status epilepticus reduces acutely hippocampal glutamate uptake and Na+/K+ ATPase activity.
pubmed:affiliation
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. losch@ufrgs.br
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't