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Assessment of the role of alpha-methylepinine in the neurotoxicity of MDMA.

T D Steele, W K Brewster, M P Johnson, D E Nichols, G K Yim

Pharmacology, biochemistry, and behavior February 1991 DOI: 10.1016/0091-3057(91)90289-e (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Preprint Peer reviewed
Population Rat and mouse liver and brain microsomes; rats receiving intracerebroventricular alpha-methylepinine
Interventions alpha-methylepinine MDMA
Duration One week following treatment
Topics MDMA
Key points The metabolite alpha-methylepinine is not solely responsible for MDMA's serotonergic neurotoxicity: its formation lacked the stereochemical preference seen with S-(+)-MDMA, and direct intracerebroventricular administration produced no persistent declines in biogenic amines or their metabolites one week later.

Abstract

To assess the potential involvement of metabolism of 3,4-methylenedioxymethamphetamine (MDMA) to the catechol alpha-methylepinine in producing serotonergic neurotoxicity, we attempted to correlate aspects of this reaction with the neurotoxicity profile of MDMA. In contrast to the stereoselectivity of S-(+)-MDMA in causing persistent declines in rat brain 5-hydroxyindole levels, no stereochemical component to the metabolic reaction was apparent. Rat liver microsomes generated a significantly greater amount of alpha-methylepinine than did mouse microsomes, but similar amounts of metabolite were produced by brain microsomes from the two species. Formation of alpha-methylepinine by hepatic, but not brain, microsomes was inhibited by SKF 525A and induced by phenobarbital, possibly indicating a tissue specificity in cytochrome P-450-dependent metabolism of MDMA. To directly assess whether alpha-methylepine is a likely mediator of MDMA neurotoxicity, the compound was administered intracerebroventricularly. No persistent declines in biogenic amines or their metabolites were observed one week following treatment. These data suggest that alpha-methylepinine alone is not responsible for the neurotoxic effects of MDMA.