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Rats were pretreated with saline or nicotine (1.5 mg/kg/day) by subcutaneously implanting each animal with an Alzet osmotic minipump which continuously released saline or nicotine (1.5 mg/kg/day) for 14 days. The behavioral and biochemical effects of nicotine on the dopaminergic neuronal system in rat nucleus accumbens were examined. It was found that chronic nicotine treatment increased the affinity of L-[3H]nicotine binding site in the nucleus accumbens. This treatment also potentiated the ability of (+)-amphetamine, but not high potassium, to stimulate formation and release of [3H]dopamine in tissue slices from rat nucleus accumbens. Chronic nicotine treatment did not alter the characteristics of [3H]spiperone binding site, the rate of dopamine turnover and the concentrations of gamma-aminobutyric acid in the nucleus accumbens.
Y K Fung, and
Y S Lau
January 1992,
Psychopharmacology,
Y K Fung, and
Y S Lau
August 1989,
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Y K Fung, and
Y S Lau
August 1988,
The Journal of pharmacology and experimental therapeutics,
Y K Fung, and
Y S Lau
December 1985,
Brain research,
Y K Fung, and
Y S Lau
October 2020,
Brain sciences,
Y K Fung, and
Y S Lau
February 1994,
Pharmacology, biochemistry, and behavior,
Y K Fung, and
Y S Lau
June 1995,
Synapse (New York, N.Y.),
Y K Fung, and
Y S Lau
August 1988,
Neuropharmacology,
Y K Fung, and
Y S Lau
February 2021,
International journal of molecular sciences,
Y K Fung, and
Y S Lau
May 2004,
Neuroscience letters,
