Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1995-3-22
pubmed:abstractText
Disruption of the fiber connections between the temporal cortex (TC) and lateral entorhinal cortex (LEC) results in impaired memory and decrease of glutamate in both denervated areas. Administration of glutamatergic agonists fully restores the mnemonic function in rats with TC/LEC lesions. The purpose of the present study was to examine whether the pharmacologically supported recovery of function may act via NMDA receptors. Rats with TC/LEC lesions either received saline, the NMDA antagonist HA-966, the NMDA agonist glycine or HA-966 + glycine. The results show that saline-treated rats are severely impaired in retention, whereas rats treated with glycine perform like normal controls. Rats pretreated with HA-966 are not able to profit from the beneficial effects of glycine. These data support the notion that the restoration of memory function obtained by glycine in lesioned animals involves activation of NMDA receptors.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
662
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
263-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Evidence for activation of NMDA receptors when memory function is reinstated in rats with glutamatergic temporal systems disrupted.
pubmed:affiliation
Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't