Contrasting effects of dopaminergic blockade on MDMA and d-amphetamine conditioned taste aversions.

H Q Lin; Iain S. Mcgregor; D M Atrens; M J Christie; D M Jackson

doi:10.1016/0091-3057(94)90025-6

Contrasting effects of dopaminergic blockade on MDMA and d-amphetamine conditioned taste aversions.

H Q Lin, Iain S. Mcgregor, D M Atrens, M J Christie, D M Jackson

Pharmacology, Biochemistry, and Behavior February 1994 DOI: 10.1016/0091-3057(94)90025-6 (opens in new tab)

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Characteristics	Series of experiments (animal behavioral pharmacology study) Peer reviewed
Population	Rats
Interventions	MDMA d-amphetamine SCH23390 raclopride haloperidol
Dose	MDMA 1.0 mg/kg; d-amphetamine 0.5 mg/kg; SCH23390 0.3 or 0.6 mg/kg; raclopride 0.3 or 0.6 mg/kg; SCH23390 and raclopride combined both 0.3 or 0.6 mg/kg; haloperidol 0.4 mg/kg
Topics	MDMA
Key findings	The conditioned taste aversion produced by MDMA (1.0 mg/kg) was unaffected by D1 and D2 dopamine antagonists, whereas the aversion produced by d-amphetamine (0.5 mg/kg) was attenuated by combined D1/D2 blockade and by haloperidol but not by either antagonist alone. The authors suggest dopamine plays different roles in MDMA and amphetamine CTAs, and that D1 and D2 receptors independently mediate amphetamine's aversive effect.

Abstract

A series of experiments examined the role of dopamine in the conditioned taste aversion (CTA) produced by 3,4-methylenedioxymethamphetamine (MDMA) and d-amphetamine in rats. The CTA induced by MDMA (1.0 mg/kg) was unaffected by the D1 dopamine receptor antagonist SCH23390 (0.3 or 0.6 mg/kg), the D2 receptor antagonist raclopride (0.3 or 0.6 mg/kg), SCH23390 and raclopride combined (both 0.3 or 0.6 mg/kg), or the D1/D2 receptor antagonist haloperidol (0.4 mg/kg). In contrast, the CTA produced by d-amphetamine (0.5 mg/kg) was attenuated by SCH23390 and raclopride combined (both 0.3 mg/kg) as well as haloperidol (0.4 mg/kg), but not by SCH23390 (0.3 or 0.6 mg/kg) or raclopride (0.3 or 0.6 mg/kg) alone. These results suggest that dopamine plays different roles in MDMA and amphetamine CTAs, and that the D1 and D2 receptors independently mediate the aversive effect of amphetamine in CTA.

Comparable studies

Other preclinical and animal studies on MDMA, most cited first.

Study	Year	Design
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Rats (implied by typical neurochemical study context)	1987	Experimental study
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Rat brain	1987	Animal experiment
Comparison of the monoamine transporters from human and mouse in their sensitivities to psychostimulant drugs Human and mouse dopamine, norepinephrine, and serotonin transporters expressed in cells	2006	In vitro laboratory study
Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Rats	1998	Experimental study
Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Squirrel monkeys treated with MDMA	1999	Observational cohort

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