Abstract
Oxidative and/or bioenergetic stress is thought to contribute to the mechanism of neurotoxicity of amphetamine derivatives, e.g., 3,4-methylenedioxymethamphetamine (MDMA). In the present study, the effect of MDMA on brain energy regulation was investigated by examining the effect of MDMA on brain glycogen and glucose. A single injection of MDMA (10-40 mg/kg, s.c.) produced a dose-dependent decrease (40%) in brain glycogen, which persisted for at least 1 h. MDMA (10 and 40 mg/kg, s.c.) also produced a significant and sustained increase in the extracellular concentration of glucose in the striatum. Subjecting rats to a cool ambient temperature of 17 degrees C significantly attenuated MDMA-induced hyperthermia and glycogenolysis. MDMA-induced glycogenolysis also was prevented by treatment of rats with the 5-hydroxytryptamine(2) (5-HT(2)) antagonists 6-methyl-1-(1-methylethyl)-ergoline-8 beta-carboxylic acid 2-hydroxy-1 methylprophyl ester maleate (LY-53,857; 3 mg/kg i.p.), desipramine (10 mg/kg i.p.), and iprindole (10 mg/kg i.p.). LY-53,857 also attenuated the MDMA-induced increase in the extracellular concentration of glucose as well as MDMA-induced hyperthermia. Amphetamine analogs (e.g., methamphetamine and parachloroamphetami...Continue Reading
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