Abstract
Administration of a dose of 15 mg/kg of the recreationally used drug 3,4-methylenedioxymethamphetamine (MDMA or “ecstasy”) to Dark Agouti rats resulted in an acute hyperthermic response which was followed 7 days later by a marked (≈45%) loss of 5-HT and its metabolite 5-HIAA in cortex, hippocampus and striatum and a similar loss of [3H]-paroxetine binding in cortex. These losses reflect the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. Administration of pentobarbitone (40 mg/kg) concurrently with MDMA produced a significant attenuation of the neurotoxic damage, but also acute hypothermia. When the temperature of the MDMA plus pentobarbitone-treated group was kept elevated to that of the MDMA-treated group by the use of a homeothermic blanket, the neuroprotective effect of pentobarbitone was lost. These data demonstrate that pentobarbitone appears to possess no intrinsic neuroprotective activity and the previously reported activity is due to a hypothermic action of the drug.
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Received: 12 July 1998/Final version: 29 September 1998
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Colado, M., Esteban, B., O’Shea, E. et al. Studies on the neuroprotective effect of pentobarbitone on MDMA-induced neurodegeneration. Psychopharmacology 142, 421–425 (1999). https://doi.org/10.1007/s002130050908
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DOI: https://doi.org/10.1007/s002130050908