The rise of body temperature induced by the stimulation of dopamine D 1 receptors is increased in acutely reserpinized mice

Abstract

In naive mice, the selective D 1 agonist, SK & F 38393 (7.5–30 mg/kg s.c.), induced a significant rise of body temperature (0.51°C) which was antagonized by SCH 23390 (100 μg/kg s.c.) and by flupenthixol (0.4 mg/kg i.p.). In mice treated with reserpine (5 mg/kg s.c.) 18 h before testing, which on its own caused intense hypothermia (10–12°C), SK & F 38393 (1.87–30 mg/kg s.c.) induced a dose-dependent and more marked rise of body temperature (5–7°C). Similarly, SK&F 38393 (30 mg/kg s.c.) partially prevented reserpine-induced hypothermia. The central origin of the SK&F 38393 effects in reserpine-treated mice is indicated by the rise of body temperature induced by the i.c.v. administration of the drug (12.5–50 μg per mice). The SK&F 38393-induced rise of body temperature in acutely reserpinized mice was antagonized by SCH 23390 (50–200 μg/kg s.c.), clozapine (1.87–30 mg/kg i.p.) or chlorpromazine (2–32 mg/kg i.p.) but not by metoclopramide (25 or 100 mg/kg i.p.) or amisulpride (12.5 or 50 mg/kg). In naive mice, apomorphine (1 mg/kg s.c.) or LY 171555 (0.4 mg/kg s.c.) induced hypothermia which was antagonized by amisulpride (12.5 mg/kg i.p.); a transiently increased body temperature was even measured 30 min after apomorphine injection in amisulpride-treated mice. Apomorphine (1 mg/kg s.c.) induced a rise of body temperature in acutely reserpinized mice which was significantly reduced by SCH 23390 (50 and 200 μg/kg s.c.) and significantly increased by amisulpride (12.5 and 50 mg/kg i.p.). These data suggest that pharmacologically different dopamine receptor subtypes mediate different effects on body temperature in mice: D 1 dopamine receptors mediate a rise of body temperature which is increased in hypothermic reserpinized animals and dopamine receptors of the D 4 subtype mediate the decrease of body temperature in naive mice.