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Journal of Neuroscience, Vol 7, 1093-1106, Copyright © 1987 by Society for Neuroscience
Adrenalectomy-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons: anatomic, peptide, and steroid specificity
PE Sawchenko
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.
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