Abstract

Alpha-melanocyte stimulating hormone (α-MSH), a putative endogenous antipyretic agent, is synthesized largely within neurons in the arcuate nucleus. To test the hypothesis that destruction of this area would increase the febrile response, male Wistar rats, treated as neonates with intraperitoneal injections of monosodium glutamate (MSG) or saline, were given intracerebroventricular (i.c.v.) injections of prostaglandin E 1 (20 ng; 200 ng) or purified interleukin-1 (20 U) and body temperature was monitored. The fevers displayed by the MSG-treated animals were significantly greater (P < 0.05) than those of the controls for the lower dose of PGE 1 at 10–30 min and for IL-1 at 3–6 h after the injections. MSG-treated rats showed significant reduction (P < 0.01) in α-MSH content of the medial basal hypothalamus and lateral septum when compared to saline controls. Body temperature response of non-febrile animals to high ambient temperature was not affected by the MSG treatment. These data support the hypothesis that α-MSH is an endogenous antipyretic in the rat.

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