Evidence for a local site of action for glucocorticoids in inhibiting CRF and vasopressin expression in the paraventricular nucleus.
Local intracerebral implants of the synthetic glucocorticoid, dexamethasone, prevented the expected adrenalectomy-induced enhancement of both corticotropin-releasing factor (CRF) and vasopressin immunoreactivity in parvocellular neurosecretory neurons of the paraventricular nucleus of the hypothalamus (PVH). Control experiments employing either cholesterol-filled cannulae aimed at the PVH, or dexamethasone-filled cannulae aimed at parts of the septum, amygdala or basomedial hypothalamus were ineffective in this paradigm. Coupled with recent evidence for existence of glucocorticoid receptors on CRF-containing neurons in the PVH, the results suggest that the inhibitory effect of glucocorticoids on the expression of both CRF and vasopressin in the parvocellular neurosecretory system can be mediated by receptors on the peptide-synthesizing neurons, themselves.
D000818:Animals; D002784:Cholesterol / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism*; D003907:Dexamethasone / Q000494:pharmacology*; D004343:Drug Implants; D008297:Male; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000187:drug effects; D014667:Vasopressins / Q000378:metabolism*
D004343:Drug Implants; D011965:Receptors, Glucocorticoid; D014667:Vasopressins; D003907:Dexamethasone; D003346:Corticotropin-Releasing Hormone; D002784:Cholesterol