Febrile effects of polyriboinosinic acid: polyribocytidylic acid and interferon: relationship to somatostatin in rat hypothalamus

The changes in thermoregulatory effectors produced by an injection of polyriboinosinic acid: polyribocytidylic acid (Poly I:C) or interferon were assessed and compared in control rats, in rats with hypothalamic somatostatin (SS) receptor blockade and in rats with hypothalamic SS depletion. Intrahypothalamic (i.h., 0.05–0.50 μg) or intraperitoneal (i.p., 100–600 μg) administration of Poly I:C caused a dose-related rise in colon temperature in control rats at all ambient temperatures (T_a) studied. A Poly I:C-induced fever was produced by increased metabolism at a T_a of 8 °C, whereas at 30 °C, it was caused by cutaneous vasoconstriction. At a T_a of 22 °C, the fever was caused by increased metabolism and cutaneous vasoconstriction. On the other hand, i.h. administration of SS-14 antagonist (0.1–0.5 ng) caused a dose-related fall in colon temperature at T_a of 8 °C or 22 °C. At a T_a of 8 °C, the hypothermia was caused by decreased metabolism, whereas at 22 °C, it was caused by decreased metabolism and cutaneous vasodilation. At a T_a of 30 °C, the thermoregulatory effectors were not affected by SS-14 antagonist treatment. Furthermore, the fever induced by Poly I:C or interferon was significantly reduced by pretreatment of rats with an i.p. dose of cysteamine (30 mg. kg⁻¹) or an i.h. dose of SS-14 antagonist (0.1 ng). The results indicate that a somatostatinergic pathway in rat hypothalamus may mediate the fever induced by interferon or its inducer Poly I:C.