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Treadmill running restores MDMA-mediated hyperthermia prevented by inhibition of the dorsomedial hypothalamus.

Dmitry V Zaretsky, Maria V Zaretskaia, Pamela J Durant, Daniel E. Rusyniak

Brain Research May 22, 2015 DOI: 10.1016/j.brainres.2015.02.037 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Randomized controlled trial Peer reviewed
Population Rats
Interventions Muscimol artificial CSF MDMA
Dose Muscimol 80 pmol/100 nl; MDMA 7.5 mg/kg, i.v.
Topics MDMA
Keywords Dorsomedial hypothalamus Heat stroke Hyperthermia Locomotion
Key findings A fixed treadmill exercise load abolished the decreases in temperature and mortality previously seen with DMH inhibition in freely moving rats given MDMA. The authors conclude that locomotion mediated by neurons in the DMH is critical to the development of hyperthermia from MDMA.

Abstract

The contribution of exercise to hyperthermia mediated by MDMA is not known. We recently showed that inhibiting the dorsomedial hypothalamus (DMH) attenuated spontaneous locomotion and hyperthermia and prevented deaths in rats given MDMA in a warm environment. The goal of this study was to confirm that restoring locomotion through a treadmill would reverse these effects thereby confirming that locomotion mediated by the DMH contributes to MDMA-mediated hyperthermia. Rats were randomized to receive bilateral microinjections, into the region of the DMH, of muscimol (80pmol/100nl) or artificial CSF followed by a systemic dose of either MDMA (7.5mg/kg, i.v.) or saline. Immediately after the systemic injection, rats were placed on a motorized treadmill maintained at 32°C. Rats were exercised at a fixed speed (10m/min) until their core temperature reached 41°C. Our results showed that a fixed exercise load abolished the decreases in temperature and mortality, seen previously with inhibition of the DMH in freely moving rats. Therefore, locomotion mediated by neurons in the DMH is critical to the development of hyperthermia from MDMA.

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