Regulation of hippocampal alpha1d adrenergic receptor mRNA by corticosterone in adrenalectomized rats.
The hippocampal formation receives extensive noradrenergic projections and expresses high levels of mineralocorticoid (MR) and glucocorticoid (GR) receptors. Considerable evidence suggests that the noradrenergic system influences hippocampal corticosteroid receptors. However, there is relatively little data describing the influence of glucocorticoids on noradrenergic receptors in the hippocampal formation. alpha1d adrenergic receptor (ADR) mRNA is expressed at high levels in the hippocampal formation, within cells that express MR or GR. In order to determine whether expression of alpha1d ADR mRNA is influenced by circulating glucocorticoids, male rats underwent bilateral adrenalectomy (ADX) or sham surgery, and were killed after 1, 3, 7 or 14 days. Levels of alpha1d ADR mRNA were profoundly decreased in hippocampal subfields CA1, CA2 and CA3 and the medial and lateral blades of the dentate gyrus, as early as 1day after ADX, as determined by in situ hybridization. The effect was specific for the hippocampal formation, with levels of alpha1d mRNA unaltered by ADX in the lateral amygdala, reticular thalamic nucleus, retrosplenial cortex or primary somatosensory cortex. Additional rats underwent ADX or sham surgery and received a corticosterone pellet (10 or 50mg) or placebo for 7 days. Corticosterone replacement prevented the ADX-induced decrease in hippocampal alpha1d ADR mRNA, with the magnitude of effect depending on corticosterone dose and hippocampal subregion. These data indicate that alpha1d ADR mRNA expression in the hippocampal formation is highly sensitive to circulating levels of corticosterone, and provides further evidence for a close interaction between glucocorticoids and the noradrenergic system in the hippocampus.
Psychology Department and Center for Neuroscience, University of Colorado, Boulder, CO 80309-0345, USA. heidi.day@colorado.edu
Heidi E W
HE
Day
Elisa M
EM
Kryskow
Stanley J
SJ
Watson
Huda
H
Akil
Serge
S
Campeau
D000315:Adrenalectomy; D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics* / Q000378:metabolism; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D003345:Corticosterone