Nicotine-conditioned locomotor activity in rats: dopaminergic and GABAergic influences on conditioned expression

Nicotine-Associated Cues Maintain Nicotine-Seeking Behavior in Rats Several Weeks after Nicotine Withdrawal: Reversal by the Cannabinoid (CB1) Receptor Antagonist, Rimonabant (SR141716)

“…As expected, the D 1 dopamine antagonist SCH23390 (0.01 and 0.03 mg/kg) was found to reduce responding for conditioned cues. At the lowest dose, the drug has been shown to reduce locomotor activity induced by nicotine or by nicotine-associated cues without impairing motor performance (O'Neill et al, 1991;Bevins et al, 2001). Functional imaging studies in nicotine-and cocainedependent individuals have shown that exposure to drugrelated stimuli elicits craving and activates brain regions associated with arousal, compulsive repetitive behaviors, sensory integration, and episodic memory (Brody et al, 2002;Childress et al, 1999).…”

Behavioral and neuropharmacological characterization of nicotine as a conditional stimulus

“…Rats were then given an injection of their training dose of nicotine for the next 3 days in the home cage in order to attenuate the initial locomotor suppressant effects of nicotine (Besheer et al, 2004 andBevins et al, 2001). Daily training sessions began the day following the last nicotine injection.…”

“…For example, repeated pairings of a conditional stimulus such as a chamber or fl avor with a nicotine unconditioned stimulus can produce a place preference (Fudala et al, 1985, Shoaib et al, 1994aand Shoaib et al, 1994b, taste aversion Williamson, 1984 andKumar et al, 1983), or conditioned hyperactivity (Bevins and Palmatier, 2003, Bevins et al, 2001, Shoaib et al, 1994a, Shoaib et al, 1994band Walter and Kuschinsky, 1989 in rats. More recently, systemic nicotine has been found to serve as a positive drug feature (occasion setter) indicating when a discrete light conditional stimulus will be followed by brief access to liquid sucrose and Palmatier et al, 2005.…”

“…For example, SCH-23390 is a dopamine D 1 receptor antagonist (Andersen and Grønvald, 1986, Hyttel and Arnt, 1987and Iorio et al, 1983) that blocks nicotine-induced increases of dopamine in the nucleus accumbens (Sziráki et al, 1998). SCH-23390 has also been found to block the expression of nicotineconditioned hyperactivity without affecting activity in controls (Bevins et al, 2001) and to reverse nicotine-induced lowering of brain reward thresholds (Harrison et al, 2002). When eticlopride, a dopamine D 2 / D 3 receptor antagonist (Hall et al, 1985, Köhler et al, 1986and Tang et al, 1994, is infused into the ventral tegmental area, nicotine-induced increases in dopamine in the nucleus accumbens are partially inhibited (Sziráki et al, 2002).…”

Treating cocaine addiction: From preclinical to clinical trial experience with γ‐vinyl GABA

“…More recently, Xi and Stein (2000) demonstrated that GVG blocked heroin self-administration while Bevins et al (2001) demonstrated that it partially blocked the expression of nicotine-induced locomotor activity. Wegelius et al (1993) demonstrated that GVG decreased voluntary alcohol consumption in alcohol-preferring rats and Stromberg et al (2001) established that GVG, at doses of 100, 200, and 300 mg/kg, reduced both ethanol and cocaine consumption in a dose-related manner.…”