EFFECTS OF CORTICOSTERONE ON CRH MESSENGER-RNA AND CONTENT IN THE BEDNUCLEUS OF THE STRIA TERMINALIS - COMPARISON WITH THE EFFECTS IN THE CENTRAL NUCLEUS OF THE AMYGDALA AND THE PARAVENTRICULAR NUCLEUS OF THEHYPOTHALAMUS

We previously reported that corticosterone (CORT) increased corticotro pin-releasing hormone (CRH) mRNA in the central nucleus of the amygdal a (CEA), while reducing it in the paraventricular nucleus (PVN) of the hypothalamus by using in situ hybridization histochemistry. The bed n ucleus of the stria terminalis (BNST) is closely related to the amygda la, and it is also a source of extrahypothalamic CRH; therefore, we ex amined CRH mRNA changes in the BNST following systemic treatment with CORT in adrenally-intact rats. Effects of adrenalectomy on CRH mRNA in the BNST, PVN and CEA were also examined. In addition, CRH content in these nuclei and in the median eminence (ME) were determined by micro punch dissection technique combined with CRH radioimmunoassay in CORT pellet implanted rats. Subcutaneous injections of high CORT (5 mg/day, over 14 days) increased CRH mRNA in the dorsal part of the lateral BN ST (BSTLD) at 2, 4 and 8 days, although the low dose of CORT (1 mg/kg/ day) had no significant effects. By contrast, in the ventral part of t he BNST (BSTV) neither the high nor low dose of CORT altered CRH mRNA levels. In a second experiment, a slowly-releasing CORT pellet (200 mg , 60-day release) ,produced an elevation of CRH mRNA at both 1 and 2 w eeks or at 1 week in the BSTLD or in the BSTV, respectively. These res ults show that glucocorticoids can facilitate CRH mRNA expression in t he BSTLD in the same manner as seen in the CEA, and that CRH mRNA in t he BSTLD can respond to CORT more than in the BSTV. In a third experim ent, bilateral adrenalectomy, however, did not affect CRH mRNA in the BNST although there was a modest decrease in the CEA and a robust incr ease in the PVN. Finally, in CORT pellet (200 mg, for 2 weeks) implant ed rats, CRH content in the ME significantly decreased and modestly in creased in the CEA compared with control rats, whereas it did not chan ge in the PVN and BNST. Taken together, these results suggest that (1) CRH in the BNST and the CEA may share some common functions in neuroe ndocrine and behavioral changes, but that (2) mechanisms of CRH synthe sis or its releasing sites may be different in the BNST and CEA.