Effects of catecholamine-depleting medullary knife cuts on corticotropin-releasing factor and vasopressin immunoreactivity in the hypothalamus of normal and steroid-manipulated rats.
Single and dual immunohistochemical staining techniques were used to assay the effects of disruption of brain stem catecholaminergic inputs on corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) immunoreactivity in parvocellular neurosecretory neurons of the paraventricular nucleus of the hypothalamus (PVH) in normal and in adrenalectomized (ADX) rats treated with dexamethasone or vehicle. The results may be summarized as follows: (1) In adrenally intact rats, confirmed unilateral transection of ascending catecholaminergic pathways near their origins in the medulla produced a decrement in the number of CRF-immunoreactive cells that could be detected on the side of the brain ipsilateral to the cut. No effect on AVP immunoreactivity in the parvocellular division of the PVH was evident. Staining for both peptides in terminals in the external lamina of the median eminence tended to show modest decreases on the lesioned side of the brain. Compatible results were obtained in comparing the effects of bilateral transections with controls. (2) Unilaterally lesioned ADX rats treated with vehicle showed the expected enhancement in CRF immunostaining in the parvocellular division of the PVH, though the response on the side ipsilateral to the lesion was blunted relative to that seen contralaterally; the effect of ADX on AVP immunoreactivity on the ipsilateral side was more markedly reduced, but still showed evidence of enhancement (i.e., could be colocalized in some CRF immunoreactive perikarya). (3) Unilaterally lesioned ADX rats treated with dexamethasone showed no evidence of enhanced CRF or AVP immunoreactivity in perikarya or terminals on either side of the brain. The generally lower levels of staining for both peptides seen on the lesioned side across conditions suggest that the effect of interruption of ascending catecholaminergic pathways on peptide dynamics in the PVH is dissimilar to that of ADX, is manifested via different mechanisms, and that at least some types of feedback inhibition of corticotropin-releasing peptides by adrenal steroids do not require intact catecholaminergic inputs to be exhibited.
Sawchenko
P E
PE
Salk Institute for Biological Studies, Calif.
D000311:Adrenal Glands / Q000502:physiology; D000315:Adrenalectomy; D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D001933:Brain Stem / Q000601:surgery*; D002395:Catecholamines / Q000172:deficiency / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism*; D003907:Dexamethasone / Q000008:administration & dosage; D005455:Fluorescent Antibody Technique; D006651:Histocytochemistry; D007031:Hypothalamus / Q000187:drug effects* / Q000502:physiology; D007120:Immunochemistry; D008297:Male; D008526:Medulla Oblongata / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D013194:Staining and Labeling
D002395:Catecholamines; D001127:Arginine Vasopressin; D003907:Dexamethasone; D003346:Corticotropin-Releasing Hormone