The Journal of pharmacology and experimental therapeuticsMar 22, 2003

Role of the hormone and stress systems in Ecstasy-induced high body temperature

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Updated Apr 5, 2026

Abstract

MDMA (40 mg/kg) caused a significant increase in rectal and skeletal muscle temperatures in rats, lasting for at least 3 hours post-treatment.

Hypophysectomized and thyroparathyroidectomized rats treated with MDMA did not become hyperthermic and instead experienced significant hypothermia.
These HYPO and TX rats were also resistant to the neurotoxic effects of MDMA, as indicated by serotonin measurements taken 4 to 7 days later.
MDMA treatment resulted in a significant increase in thyroxine levels one hour after administration.
Thyroid hormone replacement in TX animals restored the hyperthermic response to MDMA.
Prazosin and cyanopindolol, administered before MDMA, significantly reduced the increases in rectal and skeletal muscle temperatures, respectively.
The study suggests that MDMA-induced thermogenesis is influenced by the hypothalamic-pituitary-thyroid axis and the sympathetic nervous system, with different regulatory mechanisms for core and muscle temperature.

Simplified

An acute and potentially life-threatening complication associated with the recreational use of the 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) is hyperthermia. In the present study, Sprague-Dawley rats treated with MDMA (40 mg/kg s.c.) responded with a significant increase (maximal at 1 h) in rectal and skeletal muscle temperatures that lasted for at least 3 h post-treatment. Hypophysectomized (HYPO) and thyroparathyroidectomized (TX) animals treated with MDMA (40 mg/kg s.c.) did not become hyperthermic and in fact displayed a significant hypothermia. The HYPO and TX animals were also resistant to the serotonergic neurotoxic effects of MDMA assessed by serotonin measurements 4 to 7 days later in the striatum and hippocampus. MDMA (40 mg/kg s.c.) induced a significant increase in thyroxine levels 1 h post-treatment. Thyroid hormone replacement in TX animals returned the hyperthermic response seen after MDMA. Prazosin, an alpha(1)-antagonist (0.2 mg/kg i.p.), administered 30 min before MDMA significantly attenuated the MDMA-induced increase in rectal temperature, but had no effect on skeletal muscle temperature. Cyanopindolol, a beta(3)-antagonist (4 mg/kg s.c.), administered 30 min before MDMA (40 mg/kg s.c.) significantly attenuated the increase in skeletal muscle temperature, but had no effect on the rise in rectal temperature. The combination of prazosin and cyanopindolol resulted in an abolishment of MDMA-induced hyperthermia. The mechanisms of thermogenesis induced by MDMA seem to result from an interaction between the hypothalamic-pituitary-thyroid axis and the sympathetic nervous system, wherein mechanisms leading to core and skeletal muscle hyperthermia after MDMA exposure seem to be differentially regulated by alpha(1)- and beta(3)-adrenergic receptors.

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Role of the hormone and stress systems in Ecstasy-induced high body temperature

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