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Neurotoxicity of Methamphetamine and 3,4-methylenedioxymethamphetamine

Laura E. Halpin, Stuart A. Collins, Bryan K. Yamamoto

Life Science July 24, 2013 DOI: 10.1016/j.lfs.2013.07.014 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics MDMA
Citations 195
Key findings Methamphetamine and MDMA produce persistent damage to dopamine and serotonin nerve terminals through mechanisms including excitotoxicity, mitochondrial damage, and oxidative stress.

Abstract

Amphetamines are a class of psychostimulant drugs that are widely abused for their stimulant, euphoric, empathogenic and hallucinogenic properties. Many of these effects result from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, methamphetamine and 3,4 methylenedioxymethamphetamine (MDMA) produce persistent damage to dopamine and serotonin nerve terminals. This review summarizes the numerous interdependent mechanisms including excitotoxicity, mitochondrial damage and oxidative stress that have been demonstrated to contribute to this damage. Emerging non-neuronal mechanisms by which the drugs may contribute to monoaminergic terminal damage, as well as the neuropsychiatric consequences of this terminal damage are also presented. Methamphetamine and 3,4-methylenedioxymethamphetamine (MDMA) have similar chemical structures and pharmacologic properties compared to other abused substances including cathinone (khat), as well as a relatively new class of novel synthetic amphetamines known as ‘bath salts’ that have gained popularity amongst drug abusers.

Comparable studies

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