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Neurotoxicity profiles of substituted amphetamines in the C57BL/6J mouse.

J P O'Callaghan, D B Miller

Journal of Pharmacology and Experimental Therapeutics August 1, 1994 DOI: 10.1016/s0022-3565(25)22433-8 (opens in new tab)

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Characteristics Experimental animal study Peer reviewed
Population C57BL6/J mice
Interventions d-Methamphetamine d-Methylenedioxyamphetamine (d-MDA) d-Fenfluramine
Dose d-METH 10 mg/kg, d-MDA 20 mg/kg, d-MDMA 20 mg/kg, d-FEN 25 mg/kg, each every 2 hr for four s.c. injections
Duration Four injections every 2 hr; GFAP effects resolved by 3 weeks; cortical 5-HT decrements from d-FEN lasted weeks
Measures Glial fibrillary acidic protein (GFAP), silver degeneration stain, tyrosine hydroxylase (TH), dopamine (DA), 5-HT, core temperature
Keywords Corpus striatum Cerebral cortex Animals Mice, inbred c57bl Amphetamines Dizocilpine maleate Body temperature Dose-response relationship, drug Kinetics Female
Key findings d-Methamphetamine, d-MDA, and d-MDMA produced persistent striatal damage in mice: a 300% GFAP increase that resolved by 3 weeks and a 50-75% decrease in tyrosine hydroxylase and dopamine that did not resolve, with silver-stained fiber and terminal degeneration. d-Fenfluramine did not affect striatal parameters but caused prolonged (20%) cortical serotonin reductions without cortical GFAP changes. The authors conclude the three amphetamines, but not d-fenfluramine, damage neural elements of mouse striatum and cortex.

Abstract

Dopaminergic (DA) and serotonergic (5-HT) projections to striatum and cortex have been implicated as the primary targets of substituted amphetamine (AMP)-induced neurotoxicity, largely on the basis of the propensity of these compounds to cause protracted decrements in DA and 5-HT rather than on the basis of AMP-induced alterations of indices linked to neural damage. Moreover, most studies of AMP-induced neurotoxicity, regardless of the endpoints assessed, have been conducted using a rat model; relatively little attention has been focused on the effects of these compounds in the mouse. Here, we evaluated the potential neurotoxic effects of d-methamphetamine (d-METH), d-methylenedioxyamphetamine (d-MDA), d-methylene-dioxymethamphetamine (d-MDMA) and d-fenfluramine (d-FEN) in the C57BL6/J mouse. Astrogliosis, assessed by quantification of glial fibrillary acidic protein (GFAP), was taken as the main index of AMP-induced neural damage. A silver degeneration stain also was used to obtain direct evidence of AMP-induced neuronal damage. Assays of tyrosine hydroxylase (TH), DA and 5-HT were used to assess effects on DA and 5-HT systems. Mice received d-METH (10 mg/kg), d-MDA (20 mg/kg), d-MDMA (20 mg/kg) or d-FEN (25 mg/kg) every 2 hr for a total of four s.c. injections. d-METH, d-MDA and d-MDMA caused a large (300%) increase in striatal GFAP that resolved by 3 weeks and a 50 to 75% decrease in TH and DA that did not resolve. d-METH, d-MDA and d-MDMA also caused fiber and terminal degeneration in striatum as revealed by silver staining. d-FEN did not affect any parameters in striatum. d-METH, d-MDA and d-MDMA also increased GFAP in cortex, effects that were associated with small (10-25%) and transient decrements in cortical 5-HT. d-FEN caused prolonged (weeks) decrements (20%) in cortical 5-HT but did not affect cortical GFAP. The effects of d-METH, d-MDA and d-MDMA were stereoselective and were blocked by pretreatment with MK-801. Core temperature was slightly elevated by d-METH, d-MDA and d-MDMA but was dramatically lowered by d-FEN. The data suggest that d-METH, d-MDA and d-MDMA, but not d-FEN, produce damage to neural elements of mouse striatum and cortex.

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