Dopamine Uptake Blockers Nullify Methamphetamine-induced Decrease in Dopamine Uptake and Plasma Membrane Potential in Rat Striatal Synaptosomes

Rat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic‐dependent reuptake of dopamine. The capacity for METH‐exposed nerve terminal...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2000-09, Vol.914 (1), p.187-193
Main Authors: WESTPHALEN, R. I., STADLIN, A.
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Corpus Striatum - cytology
Dopamine - metabolism
Dopamine - pharmacokinetics
Dopamine Uptake Inhibitors - pharmacokinetics
Dopamine Uptake Inhibitors - pharmacology
Drug Combinations
Membrane Potentials - drug effects
Membrane Potentials - physiology
Methamphetamine - pharmacology
Plasma - cytology
Radioligand Assay - methods
Rats
Rats, Sprague-Dawley
Synaptosomes - drug effects
Synaptosomes - physiology
Tritium - pharmacokinetics
Vinca Alkaloids - pharmacology
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Summary:Rat striatal synaptosomes showed a reduced capacity to generate a membrane potential after being exposed to methamphetamine (METH) for 1 h. As a consequence, the dopamine (DA) synaptosomes were impeded in their electrogenic‐dependent reuptake of dopamine. The capacity for METH‐exposed nerve terminals to generate a membrane potential may contribute to the ability of METH to destroy dopaminergic neurons. DA uptake inhibitors (DAUIs) were found to counteract the METH‐induced decrease in synaptosomal [3H]DA Vmax by stablizing METH‐induced reductions in PMP. Because DAUIs showed the same effects as a Na+‐channel blocker, DAUIs may prevent METH‐induced destruction of dopaminergic neurons by raising plasma membrane potential.
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2000.tb05195.x