Adrenalectomy-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons: anatomic, peptide, and steroid specificity.

Following adrenalectomy (ADX), corticotropin-releasing factor (CRF) and vasopressin immunoreactivity are jointly expressed by a population of parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus (PVH). Because these cells stain positively for CRF, but not for vasopressin, after pretreatment with colchicine, the results suggest the existence of state-dependent alterations in the expression of peptides by neuroendocrine neurons. The present study sought to determine whether other neuropeptides (e.g., neurotensin, met-enkephalin) that have been colocalized with CRF in the parvocellular division of the PVH are influenced similarly by ADX; whether the enhancement of CRF and/or vasopressin immunoreactivity after ADX is limited to neurons of the PVH; and what factors might be involved in the regulation of the expression of these peptides in the PVH. The results confirmed that CRF and vasopressin immunoreactivity are both enhanced, and may be colocalized in a substantial population of parvocellular neurosecretory neurons after ADX; no comparable enhancement of staining for met-enkephalin or neurotensin was observed. The effect of ADX on CRF immunoreactivity was not limited to cells in the PVH, as neurons in the cerebral cortex, amygdala, and the bed nucleus of the stria terminalis also showed heightened CRF immunostaining after ADX; vasopressin immunoreactivity was never colocalized with CRF in these extrahypothalamic sites. Hypophysectomy produced an enhancement of CRF and vasopressin staining in the PVH that was comparable to that seen after ADX, implicating adrenal steroids as primary regulators of peptide expression in this system. Corticosteroid replacement studies in ADX rats indicated that lower doses of dexamethasone attenuated, and higher doses essentially abolished, the expected enhancement of both CRF and vasopressin immunoreactivity after ADX. The relative potency of steroids in mitigating these effects was dexamethasone greater than corticosterone greater than deoxycorticosterone greater than aldosterone. Collectively, these results indicate that the ADX-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons is at least somewhat specific to these peptides and to this cell type. Both peptides would appear to be regulated similarly by adrenal steroids, with glucocorticoids playing a primary role.