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Hallucinogenic Amphetamine Selectively Destroys Brain Serotonin Nerve Terminals

G.a. Ricaurte, Guy K. Bryan, L. Strauss, Lewis S. Seiden, Charles R. Schuster

Science September 6, 1985 DOI: 10.1126/science.4023719 via OpenAlex

Summary

AI-generated from the abstract

The amphetamine analog MDA, which has hallucinogenic effects, causes long-lasting reductions in serotonin levels, serotonin uptake sites, and a serotonin metabolite in rat brains. Morphological evidence suggests these changes result from degeneration of serotonin nerve terminals. These findings indicate MDA is toxic to serotonin neurons in rats and raise concerns about whether MDA and similar hallucinogenic amphetamines could cause serotonin neurotoxicity in humans.

Study at a glance

Characteristics Experimental study Peer reviewed
Population Rat brain
Intervention MDA
Topics Serotonin
Keywords Amphetamine Hallucinogen Neuroscience Pharmacology
Citations 367
Key finding MDA produces selective, long-lasting reductions in serotonin markers and appears to cause degeneration of serotonin nerve terminals in rat brain.

Abstract

(±)-3,4-Methylenedioxyamphetamine (MDA), an amphetamine analog with hallucinogenic activity, produced selective long-lasting reductions in the level of serotonin, the number of serotonin uptake sites, and the concentration of 5-hydroxyindoleacetic acid in rat brain. Morphological studies suggested that these neurochemical deficits were due to serotonin nerve terminal degeneration. These results show that MDA has toxic activity for serotonin neurons in rats and raise the question of whether exposure to MDA and related hallucinogenic amphetamines can produce serotonin neurotoxicity in the human brain.

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