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 sufï¬cient 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
Synapse – Wiley
Published: Dec 1, 2001
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