Methamphetamine Rapidly Decreases Vesicular Dopamine Uptake

• Published in: Journal of neurochemistry 2000-05, Vol.74 (5), p.2221-2223
• Main Authors: Brown, Jeffrey M., Hanson, Glen R., Fleckenstein, Annette E.
• Format: Article
• Language: English
• Subjects: Animals; Corpus Striatum - cytology; Corpus Striatum - metabolism; Dopamine - pharmacokinetics; Dopamine uptake; Dopamine Uptake Inhibitors - pharmacology; Dose-Response Relationship, Drug; Male; Membrane Glycoproteins - metabolism; Membrane Transport Proteins; Methamphetamine; Methamphetamine - pharmacology; Neurons - metabolism; Neuropeptides; p-Chloroamphetamine - pharmacology; Rats; Rats, Sprague-Dawley; Serotonin Antagonists - pharmacology; Striatum; Synaptic vesicles; Synaptic Vesicles - metabolism; Tetrabenazine - analogs & derivatives; Tetrabenazine - metabolism; Vesicular Biogenic Amine Transport Proteins; Vesicular Monoamine Transport Proteins; Vesicular monoamine transporter
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1046/j.1471-4159.2000.0742221.x

: Vesicular sequestration is important in the regulation of cytoplasmic concentrations of monoamines such as dopamine. Moreover, recent evidence suggests that increases in cytoplasmic dopamine levels, perhaps attributable to changes in vesicular monoamine transporter function, contribute to methamphetamine‐induced dopaminergic deficits. Hence, we examined whether striatal vesicular uptake is altered following methamphetamine treatment. Multiple administrations of methamphetamine rapidly (within 1 h) decreased vesicular dopamine uptake and dihydrotetrabenazine binding, an effect that (a) persisted at least 24 h, (b) was associated with dopamine and not serotonin neurons, and (c) was unrelated to residual drug introduced by the original methamphetamine treatment. These data suggest that methamphetamine rapidly decreases vesicular monoamine transporter function in dopaminergic neurons, a phenomenon that may be associated with the long‐term damage caused by this stimulant.