A possible role of hypothalamic somatostatin in the maintenance of rat pituitary responsiveness to growth hormone-releasing factor.
To characterize the role of hypothalamic somatostatin (SRIF) in regulating pituitary responsiveness to GH-releasing factor (GRF) in vitro, we reduced SRIF input to the rat anterior pituitary through the portal vessels. Three different paradigms were used as follows: 1) anterolateral hypothalamic deafferentation, 2) electrolytic lesions of the periventricular nucleus, and 3) passive immunization with SRIF antiserum. Rat CRF content in the stalk-median eminence markedly decreased to 19% and 57% of that of sham-operated controls 10 days after the deafferentation and the lesions, respectively. In contrast, rat GRF content was unchanged by either operation. SRIF content markedly decreased to 78%, 12%, and 2% of the control level 1, 3, and 10 days after deafferentation, respectively, and to 48% and 8%, 1 and 10 days after the lesions, respectively. The serum GH concentration was significantly increased 1 and 3 days after the deafferentation (P less than 0.01) and also 1 day after the lesions (P less than 0.01), followed by no increase 10 days after either operation. Anterior pituitary weight and GH content markedly decreased 3 and 10 days and 10 days after the deafferentation and the lesions, respectively. The human GRF (0.1 microM)-induced GH release response of anterior pituitaries removed from these treated rats was examined in an in vitro perifusion system. Even 1 day after these treatments, GH responsiveness was clearly attenuated by anterolateral hypothalamic differentiation (8.61 +/- 0.78 vs. 3.62 +/- 0.54 micrograms GH/h; P less than 0.01), periventricular nucleus lesions (6.52 +/- 1.07 vs. 3.20 +/- 0.53 micrograms GH/h; P less than 0.01) and passive immunization with SRIF antiserum (5.80 +/- 0.43 vs. 2.54 +/- 0.16 micrograms GH/h; P less than 0.01). This attenuated responsiveness gradually deteriorated 3 and 10 days after the surgical operations. These results indicate that SRIF neurons in the anterior periventricular nucleus play a role in maintaining the pituitary responsiveness to GRF, in addition to the original action of inhibiting GH release.
Soya
H
H
Department of Physiology, Gunma University, Maebashi, Japan.
Suzuki
M
M
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D003714:Denervation; D013006:Growth Hormone / Q000378:metabolism; D013007:Growth Hormone-Releasing Hormone / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D007031:Hypothalamus / Q000378:metabolism*; D007032:Hypothalamus, Anterior / Q000502:physiology; D007106:Immune Sera / Q000276:immunology; D007116:Immunization, Passive; D008297:Male; D008473:Median Eminence / Q000378:metabolism; D010902:Pituitary Gland / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000276:immunology / Q000378:metabolism / Q000502:physiology*
D007106:Immune Sera; D013004:Somatostatin; D013006:Growth Hormone; D003346:Corticotropin-Releasing Hormone; D013007:Growth Hormone-Releasing Hormone