Iptakalim Inhibits Nicotine-Induced Enhancement Of Extracellular Dopamine And Glutamate Levels In The Nucleus Accumbens Of Rats

Department

neurobiology

Document Type

Article

Abstract

Iptakalim (Ipt) is a novel ATP-sensitive potassium channel opener. It has been reported that Ipt inhibited cocaine-induced dopamine and glutamate release, suggesting that Ipt may regulate drug addiction. Recently, we found that Ipt blocked nicotinic acetylcholine receptor (nAChR)-mediated currents in a heterologously expressed SH-EP1 cell line and in native midbrain dopamine neurons. In the present study, we examined whether Ipt prevents nicotine-induced neurotransmitter release in the nucleus accumbens (NAc) using in vivo microdialysis methods in awake, freely moving rats. Ipt was administered through a microdialysis probe, following systemic administration of nicotine (0.5 mg/kg, s.c.). The results show that acute nicotine treatment induced an increase of both dopamine and glutamate levels in the rat NAc, and that Ipt significantly attenuated nicotine's effects in a concentration-dependent manner. Therefore, Ipt may serve as a novel compound to block nicotine-induced dopamine and glutamate release in the brain reward center, in turn decreasing nicotine reinforcement and dependence. © 2006 Elsevier B.V. All rights reserved.

Publication Date

4-26-2006

Publication Title

Brain Research

ISSN

00068993

Volume

1085

Issue

1

First Page

138

Last Page

143

Digital Object Identifier (DOI)

10.1016/j.brainres.2006.02.096

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