Brazell M P, Mitchell S N, Joseph M H, Gray J A
MRC Brain, Behaviour and Psychiatry Research Group, Department of Psychology, Institute of Psychiatry, London, U.K.
Neuropharmacology. 1990 Dec;29(12):1177-85. doi: 10.1016/0028-3908(90)90042-p.
Using in vivo dialysis and voltammetry, the effect of acute administration of (-)-nicotine (0.8 mg/kg free base, s.c.) on extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid, 5-hydroxy-indoleacetic acid and ascorbic acid in the nucleus accumbens and caudate-putamen of chloral hydrate-anaesthetised rats has been examined. Nicotine stimulated release of dopamine only in the nucleus accumbens, measured using dialysis. After a short time delay levels of 3,4-dihydroxyphenylacetic acid in both the nucleus accumbens and caudate-putamen also increased. In both regions, 5-hydroxyindoleacetic acid was unaffected by nicotine. Using voltammetry the effect of nicotine on extracellular levels of 3,4-dihydroxyphenylacetic acid and ascorbic acid was examined. An increase in 3,4-dihydroxyphenylacetic acid was observed in both regions after nicotine. This increase was blocked by pretreatment with the central nicotinic receptor antagonist mecamylamine (5 mg/kg). Nicotine increased the level of ascorbic acid in the nucleus accumbens and caudate-putamen; while in animals pretreated with mecamylamine, nicotine decreased levels of ascorbate. These results show that acute administration of nicotine stimulated release of dopamine in the nucleus accumbens and increased the levels of DOPAC and ascorbic acid in the nucleus accumbens and caudate-putamen. This effect is probably mediated by nicotinic receptors as it was antagonised by mecamylamine.
运用体内透析和伏安法,研究了水合氯醛麻醉大鼠腹腔注射(-)-尼古丁(0.8mg/kg游离碱,皮下注射)对伏隔核和尾状壳核细胞外多巴胺、3,4-二羟基苯乙酸、5-羟基吲哚乙酸及抗坏血酸水平的影响。通过透析测定,尼古丁仅刺激伏隔核中多巴胺的释放。短暂延迟后,伏隔核和尾状壳核中3,4-二羟基苯乙酸的水平也升高。在这两个区域,5-羟基吲哚乙酸不受尼古丁影响。运用伏安法研究了尼古丁对细胞外3,4-二羟基苯乙酸和抗坏血酸水平的影响。尼古丁作用后,两个区域均观察到3,4-二羟基苯乙酸增加。这种增加被中枢烟碱受体拮抗剂美加明(5mg/kg)预处理所阻断。尼古丁使伏隔核和尾状壳核中抗坏血酸水平升高;而在美加明预处理的动物中,尼古丁降低了抗坏血酸水平。这些结果表明,急性给予尼古丁可刺激伏隔核中多巴胺的释放,并增加伏隔核和尾状壳核中DOPAC和抗坏血酸的水平。这种作用可能由烟碱受体介导,因为它被美加明所拮抗。