Protein synthesis blockade differentially affects the stress- induced transcriptional activation of neuropeptide genes in parvocellular neurosecretory neurons

Abstract

Corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are synergistically interacting ACTH secretagogues that are co-expressed by parvocellular neurosecretory neurons of the hypothalamic paraventricular nucleus (PVH). To shed light on the mechanisms that mediate the stress-induced transcriptional activation of these neuropeptide genes, quantitative hybridization histochemical methods were used to assess the effects of systemic treatment with the protein synthesis inhibitor, cycloheximide, on the ether stress-induced upregulation of primary CRF and AVP transcripts, in vivo. Pretreatment with cycloheximide prevented the induction of Fos, but not CREB phosphorylation, normally seen in response to acute ether exposure, and significantly attenuated the stress-induced rise in AVP, but not CRF, heteronuclear RNA expression in the parvocellular division of the PVH. These results support the view that distinct molecular mechanisms govern the expression of the two principal corticotropin-releasing factors, in vivo.