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The Journal of Neuroscience, October 1, 2002, 22(19):8705-8710

Methylphenidate Redistributes Vesicular Monoamine Transporter-2: Role of Dopamine Receptors

Verónica Sandoval, Evan L. Riddle, Glen R. Hanson, and Annette E. Fleckenstein

Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah 84112

It is well accepted that methylphenidate (MPD) inhibits dopamine (DA) transporter function. In addition to this effect, this study demonstrates that MPD increases vesicular [³H]DA uptake and binding of the vesicular monoamine transporter-2 (VMAT-2) ligand dihydrotetrabenazine (DHTBZ) in a dose- and time-dependent manner in purified striatal vesicles prepared from treated rats. This change did not result from residual MPD introduced by the original in vivo treatment, because application of MPD in vitro (1 µM) was without effect, and higher concentrations decreased vesicular [³H]DA uptake. In addition, MPD treatment increased and decreased VMAT-2 immunoreactivity in striatal vesicle subcellular and plasmalemmal membrane fractions, respectively. The MPD-induced increase in both VMAT-2 immunoreactivity and DHTBZ binding was attenuated by pretreatment in vivo with either the DA D₁ receptor antagonist SCH23390 or the DA D₂ receptor antagonist eticlopride. Coadministration of these antagonists in vivo inhibited completely the MPD-induced increase in DHTBZ binding in the purified vesicular preparation. These observations suggest a role for DA in the MPD-induced redistribution of VMAT-2. The implications of this phenomenon will be discussed.

Key words: eticlopride; SCH23390; VMAT-2; D₁ receptor; D₂ receptor; vesicle redistribution

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22198705-06$05.00/0

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