Linked Life Data

9153648

Source:http://linkedlifedata.com/resource/pubmed/id/9153648

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-7-21
pubmed:abstractText
Some of the effects of glucocorticoids on the function and neuronal plasticity of the hippocampus are mediated by N-methyl-D-aspartate receptor activation. We tested the hypothesis that chronic corticosterone administration increases N-methyl-D-aspartate receptor expression in the hippocampus of the rat. We used in situ hybridization histochemistry to measure the messenger RNA levels for the NR1, NR2A and NR2B subunits of the N-methyl-D-aspartate receptor and [3H]dizocilpine maleate (a non-competitive antagonist) binding to measure N-methyl-D-aspartate receptor density. Since corticosterone depresses circulating testosterone levels, we also examined whether the effects of corticosterone are mediated by or interact with the effects of testosterone. In the intact animal, corticosterone increased messenger RNA levels for NR2A and NR2B but not NR1 subunits of the N-methyl-D-aspartate receptor in all regions of the hippocampus. Testosterone had no significant effect on messenger RNA levels of any of the subunits. The subunit composition determines the functional and pharmacological properties of the N-methyl-D-aspartate receptor. We used ifenprodil inhibition of [3H]dizocilpine maleate binding, which has been used to distinguish NR2A- from NR2B-containing receptors, to determine whether corticosterone altered the proportion of high- and low-affinity sites for ifenprodil in parallel with the changes in subunit messenger RNA levels. Corticosterone increased the density of [3H]dizocilpine maleate binding sites without changing the dissociation constant for [3H]dizocilpine maleate or the proportion of high- and low-affinity sites for ifenprodil. These data suggest that the effects of corticosterone on hippocampal function are mediated, in part, by parallel increases in NR2A and NR2B subunit levels and the number of receptor channel binding sites.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
653-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9153648-Animals, pubmed-meshheading:9153648-Anti-Inflammatory Agents, pubmed-meshheading:9153648-Binding, Competitive, pubmed-meshheading:9153648-Binding Sites, pubmed-meshheading:9153648-Cell Membrane, pubmed-meshheading:9153648-Corticosterone, pubmed-meshheading:9153648-Dizocilpine Maleate, pubmed-meshheading:9153648-Excitatory Amino Acid Antagonists, pubmed-meshheading:9153648-Glucocorticoids, pubmed-meshheading:9153648-Hippocampus, pubmed-meshheading:9153648-Image Processing, Computer-Assisted, pubmed-meshheading:9153648-In Situ Hybridization, pubmed-meshheading:9153648-Male, pubmed-meshheading:9153648-Piperidines, pubmed-meshheading:9153648-RNA, Messenger, pubmed-meshheading:9153648-Rats, pubmed-meshheading:9153648-Rats, Sprague-Dawley, pubmed-meshheading:9153648-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:9153648-Testosterone
pubmed:year
1997
pubmed:articleTitle
Chronic corticosterone treatment induces parallel changes in N-methyl-D-aspartate receptor subunit messenger RNA levels and antagonist binding sites in the hippocampus.
pubmed:affiliation
Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't