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Studies on the effect of MDMA (‘ecstasy’) on the body temperature of rats housed at different ambient room temperatures

A Richard Green, Esther O’shea, Kathryn S. Saadat, J.m. Elliott, M. Isabel Colado

British Journal of Pharmacology July 4, 2005 DOI: 10.1038/sj.bjp.0706318 via OpenAlex

Summary

AI-generated from the abstract

In rats, MDMA (ecstasy) causes hyperthermia at normal or warm room temperatures but hypothermia in cool conditions. At 15°C, MDMA rapidly lowered rectal temperature; this effect was blocked by a dopamine D2 receptor antagonist but not a D1 antagonist. A neurotoxic MDMA regimen reduced serotonin in the brain by about 30% after a week. This serotonin lesion did not affect tail temperature increases when rats moved from 20°C to 30°C, but led to lower tail temperatures when returned to 24°C. Acute MDMA in lesioned rats at 30°C caused a sustained drop in tail temperature. The findings suggest that thermoregulatory problems in MDMA-lesioned rats stem partly from impaired heat loss through the tail, a key heat-loss organ.

Study at a glance

Characteristics Experimental study Peer reviewed
Population Rats
Interventions MDMA remoxipride SCH23390
Dose 5 mg kg−1 i.p.
Duration Acute and 7-day follow-up
Topics MDMA
Keywords Hypothermia Chemistry Hyperthermia Antagonist
Citations 70
Key finding MDMA-induced hypothermia at cool ambient temperature is mediated by dopamine D2 receptors, and prior serotonin depletion impairs tail vasodilation, a critical heat-loss mechanism.

Abstract

3,4‐Methylenedioxymethamphetamine (MDMA, ‘ecstasy’) administration to rats produces hyperthermia if they are housed in normal or warm ambient room temperature ( T a ) conditions (20°C), but hypothermia when in cool conditions ( T a 17°C). We have now investigated some of the mechanisms involved. MDMA (5 mg kg −1 i.p.) produced a rapid decrease in rectal temperature in rats at T a 15°C. This response was blocked by pretreatment with the dopamine D 2 receptor antagonist remoxipride (10 mg kg −1 i.p.), but unaltered by pretreatment with the D 1 antagonist SCH23390 (1.1 mg kg −1 i.p.). MDMA (5 mg kg −1 ) did not alter the tail temperature of rats at T a 15°C, but decreased the tail temperature of rats at T a 30°C. A neurotoxic dose of MDMA (three doses of 5 mg kg −1 given 3 h apart) decreased cortical and hippocampal 5‐HT content by approximately 30% 7 days later. This lesion did not influence the rise in tail temperature when rats were moved from T a 20°C to 30°C compared to nonlesioned controls, but did result in a lower tail temperature than that of controls when they were returned to T a 24°C. Acute administration of MDMA (5 mg kg −1 ) to MDMA‐lesioned rats produced a sustained decrease in tail temperature in rats housed at T a 30°C compared to nonlesioned controls. These data suggest that the thermoregulatory problems previously observed in MDMA‐lesioned rats housed at T a 30°C result, partially, from their inability to lose heat by vasodilation of the tail, a major heat‐loss organ in this species. British Journal of Pharmacology (2005) 146 , 306–312. doi: 10.1038/sj.bjp.0706318

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