Body Temperature Response to Cocaine and Diazepam in Morphine-Treated Rats

Abstract

Since cocaine or diazepam are used clinically and/or abused concomitantly with narcotics, this study was designed to determine if morphine-dependent, morphine-withdrawn, or acute morphine rats exhibit an altered core body temperature at 24 or 4 °C to either cocaine (10, 20, or 30 mg/kg i.p.) or diazepam (2 or 4 mg/kg i.p.). At 24 °C, each dose of cocaine manifested hyperthermia in all groups of rats except morphine-dependent whereas at 4 °C cocaine produced hypothermia in all groups except morphine-dependent. At both 24 and 4°C, diazepam, 2 or 4 mg/kg, caused a hypothermic response in control, dependent, and withdrawn animals. At 24 °C, administration of acute morphine alone induced a hyperthermia which was antagonized by both doses of diazepam. At 4°C, acute morphine alone induced an initial hypothermia followed by a hyperthermia; both doses of diazepam potentiated the hypothermic response to acute morphine. Thus, significant alterations in core body temperature may be induced following the administration of cocaine or diazepam to morphine-treated rats.

Random access to palatable food stimulates similar addiction-like responses as a fixed schedule, but only a fixed schedule elicits anticipatory activation

“…This process provides a new insight into the anticipation to PF because it suggests that the anticipatory process to PF starts much earlier than observed with the behavioral activation. Low body temperature has been reported as part of the withdrawal response in rodents that have been exposed to drugs 45,46 . Thus, in the present study this anticipatory low temperature may indicate a daily brief withdrawal process due to the restricted access.…”

Methanandamide attenuates cocaine-induced hyperthermia in rats by a cannabinoid CB1-dopamine D2 receptor mechanism

“…A lesser known effect of cocaine is the hyperthermia that it causes in humans and animals (Marzuk et al, 1998; Kalant, 2001; Wiechman and Spratto, 1982; Gonzalez, 1993; Lomax and Daniel, 1990; Hamida et al, 2008; Ansah et al, 1996). Increased dopaminergic transmission mediates cocaine-induced hyperthermia and hyperactivity (Hurd and Ungerstedt, 1989; Rockhold et al, 1991; Faunt and Crocker, 1987; Zarrindast and Tabatabai, 1992; Nagashima et al, 1992; Verma and Kulkarni, 1993), but anandamide may also play a role because its brain concentration is elevated following acute psychostimulant exposure (Thiemann et al, 2008; Centonze et al, 2004; Masserano et al, 1999).…”