EFFECTS OF ADRENAL-STEROID MANIPULATIONS AND REPEATED RESTRAINT STRESS ON DYNORPHIN MESSENGER-RNA LEVELS AND EXCITATORY AMINO-ACID RECEPTOR-BINDING IN HIPPOCAMPUS

Citation
Y. Watanabe et al., EFFECTS OF ADRENAL-STEROID MANIPULATIONS AND REPEATED RESTRAINT STRESS ON DYNORPHIN MESSENGER-RNA LEVELS AND EXCITATORY AMINO-ACID RECEPTOR-BINDING IN HIPPOCAMPUS, Brain research, 680(1-2), 1995, pp. 217-225
Citations number
38
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
680
Issue
1-2
Year of publication
1995
Pages
217 - 225
Database
ISI
SICI code
0006-8993(1995)680:1-2<217:EOAMAR>2.0.ZU;2-2
Abstract
Adrenal steroid and stress effects were determined in hippocampus on l evels of dynorphin (DYN) mRNA, expressed in dentate gyrus, and excitat ory amino acid receptors, measured in Ammon's horn and dentate gyrus. Adrenalectomy (ADX) decreased DYN mRNA levels in dentate gyrus and rep lacement with aldosterone (ALDO), a specific type I adrenal steroid re ceptor agonist, prevented the decrease. Ru28362, a specific type II re ceptor agonist, had no effect. Likewise, kainate receptor binding to t he stratum lucidum and hilus region of dorsal hippocampus was decrease d after ADX and this decrease was prevented by ALDO but not by Ru28362 treatment. Similar though smaller effects were found for CNQX binding to AMPA receptors but only in the dentate gyrus molecular or infra- a nd supragranular layers. Although corticosterone (CORT) treatment of i ntact rats (40 mg/kg for 3 weeks) elevated DYN mRNA levels in dentate gyrus, up to 14 days of daily restraint stress (1 or 6 h/day) had no s ignificant effect. Neither CORT treatment nor repeated restraint stres s altered NMDA and non-NMDA glutamate receptors in hippocampus. The re sults of this study showing ADX-induced decreases of DYN mRNA and CNQX binding in dentate gyrus and decreased kainate binding in messy fiber terminal regions are consistent with morphological evidence showing t hat adrenal steroids maintain normal integrity and structure of dentat e gyrus neurons and do so via type I adrenal steroid receptors. These same parameters are apparently not sensitive to chronic restraint stre ss although the effects of other stressors must be examined.