Alterations in the thermic response to chlorpromazine in rats exposed prenatally to central nervous system depressants.

Abstract The thermic response to acute administration of chlorpromazine (5 mg/kg, i.p.) was assessed in rats exposed prenatally to haloperidol (0.1 mg/kg), phenobarbital (10 mg/kg), nitrazepam (2 mg/kg), propylene glycol (1 ml/kg) or saline, once daily from days 1–21 or 15–21 of gestation. The response in all animals was tested only once. The administration of chlorpromazine to 8- or 13-week-old male and female rats treated with saline (1–21 d) induced marked hypothermia for a 6-hr period of observation. Male and female rats treated with haloperidol (1–21 d) showed a delayed hyperthermic response to chlorpromazine at 8 weeks of age; the males showed an increase in rectal temperature at 3 hr and the females from 3 to 6 hr. Thirteen-weck-old males but not females treated with haloperidol (1–21 d) showed a hyperthennic response to chlorpromazine during the first 2 hr. Eight-week-old male and female rats treated with phenobarbital (1–21 d) showed hypothermia, whereas 13-week-old male rats of another group treated with phenobarbital (1–21d) showed significant hyperthermia after the administration of the chlorpromazine. The hypothermic response of the rats treated with nitrazepam (1–21d) to chlorpromazine was similar to that in the vehicle (propylene glycol)-treatcd controls. The male rats treated with phenobarbital (15–21d) responded to chlorpromazine with significant hyperthermia from 30 min to 1 hr. There was no alteration in thermic response to chlorpromazine in rats born to mothers treated with one tenth of the dose of phenobarbital, haloperidol or nitrazepam. The results suggest that prenatal exposure to several central depressant drugs affects the development of the thermoregulatory system and that the acute thermic response to chlorpromazine can reveal latent abnormalities of brain function in rats after prenatal exposure to such drugs.