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Rapid ATP Loss Caused by Methamphetamine in the Mouse Striatum: Relationship Between Energy Impairment and Dopaminergic Neurotoxicity
Author(s) -
Chan Piu,
Monte Donato A.,
Luo JinJun,
DeLanney Louis E.,
Irwin Ian,
Langston J. William
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62062484.x
Subject(s) - meth , methamphetamine , dopaminergic , neurotoxicity , striatum , dopamine , chemistry , hippocampus , medicine , endocrinology , pharmacology , toxicity , monomer , organic chemistry , acrylate , polymer
To study the relationship between energy impairment and the effects of α‐methamphetamine (METH) on dopaminergic neurons, ATP and dopamine levels were measured in the brain of C57BL/6 mice treated with either a single or four injections of METH (10 mg/kg, i.p.) at 2‐h intervals. Neither striatal ATP nor dopamine concentrations changed after a single injection of METH, but both were significantly decreased 1.5 h after the multiple‐dose regimen. The effects of METH on ATP levels appear to be selective for the striatum, as ATP concentrations were not affected in the cerebellar cortex and hippocampus after either a single or multiple injections of METH. In a second set of experiments, an intraperitoneal injection of 2‐deoxyglucose (2‐DG; 1 g/kg), an inhibitor of glucose uptake and utilization, was given 30 min before the third and fourth injections of METH. 2‐DG significantly potentiated METH‐induced striatal ATP loss at 1.5 h and dopamine depletions at 1.5 h and 1 week. These results indicate that a toxic regimen of METH selectively causes striatal energy impairment and raise the possibility that perturbations of energy metabolism play a role in METH‐induced dopaminergic neurotoxicity.