The effect of the atypical antipsychotic drug, amperozide, on carrier- mediated striatal dopamine release measured in vivo

Bryan Yamamoto, H. Y. Meltzer

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

The effect of the novel atypical antipsychotic drug, amperozide, on carrier-mediated dopamine efflux was studied using in vivo microdialysis in the striatum of awake-behaving rats. Amperozide was infused directly through the dialysis probe. This local infusion produced a concentration-dependent increase in striatal dopamine overflow. This increase was attenuated when a Ca++-free perfusion medium was used. Local infusion of amperozide blocked dopamine efflux after the systemic administration of amphetamine in a concentration-dependent manner. The antagonistic effect of amperozide (50 μM) on amphetamine-induced efflux of dopamine was not attenuated under Ca++-free conditions. Similar to its effects on amphetamine-induced dopamine efflux, amperozide (50 μM) attenuated the increase in dopamine overflow produced by ouabain (10 μM) but not veratridine (15 μM). The systemic coadministration of amperozide (10 mg/kg, i.p.) and haloperidol (2 mg/kg, i.p.) increased extracellular dopamine levels in an additive manner when compared to the increases observed after the administration of either drug alone. Overall, these data indicate that amperozide acts on the dopamine transporter to inhibit carrier-mediated release.

Original languageEnglish (US)
Pages (from-to)180-185
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume263
Issue number1
StatePublished - 1992
Externally publishedYes

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Corpus Striatum
Antipsychotic Agents
Dopamine
Amphetamine
Dopamine Plasma Membrane Transport Proteins
Veratridine
Microdialysis
Haloperidol
Ouabain
amperozide
Dialysis
Perfusion
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Pharmacology

Cite this

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abstract = "The effect of the novel atypical antipsychotic drug, amperozide, on carrier-mediated dopamine efflux was studied using in vivo microdialysis in the striatum of awake-behaving rats. Amperozide was infused directly through the dialysis probe. This local infusion produced a concentration-dependent increase in striatal dopamine overflow. This increase was attenuated when a Ca++-free perfusion medium was used. Local infusion of amperozide blocked dopamine efflux after the systemic administration of amphetamine in a concentration-dependent manner. The antagonistic effect of amperozide (50 μM) on amphetamine-induced efflux of dopamine was not attenuated under Ca++-free conditions. Similar to its effects on amphetamine-induced dopamine efflux, amperozide (50 μM) attenuated the increase in dopamine overflow produced by ouabain (10 μM) but not veratridine (15 μM). The systemic coadministration of amperozide (10 mg/kg, i.p.) and haloperidol (2 mg/kg, i.p.) increased extracellular dopamine levels in an additive manner when compared to the increases observed after the administration of either drug alone. Overall, these data indicate that amperozide acts on the dopamine transporter to inhibit carrier-mediated release.",
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