Topiramate selectively attenuates nicotine‐induced increases in monoamine release

Topiramate selectively attenuates nicotine‐induced increases in monoamine release WYNNE K. SCHIFFER,1,2* MADINA R. GERASIMOV,1 DOUGLAS A. MARSTELLER,1 JUSTIN GEIGER,1 CHANNING BARNETT,1 DAVID L. ALEXOFF,1 AND STEPHEN L. DEWEY,1,2 1 Chemistry Department, Brookhaven National Laboratory, Upton, New York 2 Department of Psychiatry, NYU School of Medicine, New York, New York It is widely held that the reinforcing and dependence-producing properties of nicotine rely on activation of the mesocorticolimbic dopamine (DA) system. This notion is primarily derived from demonstrations that lesions of ventral tegmental area (VTA) DA neurons projecting to the nucleus accumbens (NAcc) can reduce both locomotor activation and the reinforcing effects of nicotine (Clarke et al., 1988; Corrigall et al., 1992). However, it appears that pharmacologically targeting isolated DA receptors is not sufficient to reduce symptoms associated with nicotine dependence (Di Chiara, 2000; Kameda et al., 2000). Recent studies suggest that N-methyl-D-aspartate (NMDA) glutamate receptor activation within the VTA may be required for nicotine to stimulate DA release in the NAcc (LeikolaPelho and Jackson, 1992; Nisell et al., 1994; Shim et al., 2001), consistent with demonstrations that microinfusion of ionotropic glutamate receptor antagonists reduces nicotine-induced increases in neurochemical and locomotor activity (Schilstrom et al., 1998; Svensson et al., 1998). It has been proposed that this effect http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Synapse Wiley

Topiramate selectively attenuates nicotine‐induced increases in monoamine release

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Publisher
Wiley
Copyright
Copyright © 2001 Wiley‐Liss, Inc.
ISSN
0887-4476
eISSN
1098-2396
DOI
10.1002/syn.10000
Publisher site
See Article on Publisher Site

Abstract

WYNNE K. SCHIFFER,1,2* MADINA R. GERASIMOV,1 DOUGLAS A. MARSTELLER,1 JUSTIN GEIGER,1 CHANNING BARNETT,1 DAVID L. ALEXOFF,1 AND STEPHEN L. DEWEY,1,2 1 Chemistry Department, Brookhaven National Laboratory, Upton, New York 2 Department of Psychiatry, NYU School of Medicine, New York, New York It is widely held that the reinforcing and dependence-producing properties of nicotine rely on activation of the mesocorticolimbic dopamine (DA) system. This notion is primarily derived from demonstrations that lesions of ventral tegmental area (VTA) DA neurons projecting to the nucleus accumbens (NAcc) can reduce both locomotor activation and the reinforcing effects of nicotine (Clarke et al., 1988; Corrigall et al., 1992). However, it appears that pharmacologically targeting isolated DA receptors is not sufficient to reduce symptoms associated with nicotine dependence (Di Chiara, 2000; Kameda et al., 2000). Recent studies suggest that N-methyl-D-aspartate (NMDA) glutamate receptor activation within the VTA may be required for nicotine to stimulate DA release in the NAcc (LeikolaPelho and Jackson, 1992; Nisell et al., 1994; Shim et al., 2001), consistent with demonstrations that microinfusion of ionotropic glutamate receptor antagonists reduces nicotine-induced increases in neurochemical and locomotor activity (Schilstrom et al., 1998; Svensson et al., 1998). It has been proposed that this effect

Journal

SynapseWiley

Published: Dec 1, 2001

References

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