Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-9-23
pubmed:abstractText
Exposure to an acute stressful event facilitates classical eye-blink conditioning in the male rat. The facilitation persists for days after the stressor and its induction is prevented by antagonism of the N-methyl-D-aspartate (NMDA) type of glutamate receptor. To determine whether NMDA receptor antagonists prevent the facilitated conditioning by activity in the amygdala, a competitive antagonist, AP5, was injected bilaterally into the lateral/basolateral versus central nuclei of the amygdala. Local injection of D,L-2-amino-5-phosphonovaleric acid (AP5) into the lateral/basolateral nucleus before stressor exposure prevented the facilitated learning 24 hr later, whereas antagonism in the central nucleus before stressor exposure did not. To determine when the necessary activation occurs, AP5 was injected into the lateral/basolateral nucleus before versus after exposure to the acute stressful event. Blockade of NMDA receptors before but not after stressor exposure prevented the facilitated acquisition of the conditioning in response to stress. These results suggest that exposure to a stressful event transiently activates NMDA receptors in basolateral/lateral nuclei of the amygdala and thereby induces a persistent enhancement of associative learning.
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1072-0502
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-30
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:articleTitle
NMDA receptor antagonism in the lateral/basolateral but not central nucleus of the amygdala prevents the induction of facilitated learning in response to stress.
pubmed:affiliation
Department of Psychology and Center for Neuroscience, Rutgers University, Piscataway, New Jersey 08903, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't