Iptakalim Inhibits Nicotine-Induced Enhancement Of Extracellular Dopamine And Glutamate Levels In The Nucleus Accumbens Of Rats
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 (0.5Â 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. Â© 2006 Elsevier B.V. All rights reserved.
Digital Object Identifier (DOI)
Liu, Qiang; Li, Zhen; Ding, Jian Hua; Liu, Su Yi; Wu, Jie; and Hu, Gang, "Iptakalim Inhibits Nicotine-Induced Enhancement Of Extracellular Dopamine And Glutamate Levels In The Nucleus Accumbens Of Rats" (2006). Translational Neuroscience. 154.