作者: S. Singer , S. Rossi , S. Verzosa , A. Hashim , R. Lonow
DOI: 10.1023/B:NERE.0000035814.45494.15
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摘要: Nicotine, one of the most widespread drugs abuse, has long been shown to impact areas brain involved in addiction and reward. Recent research, however, begun explore positive effects that nicotine may have on learning memory. The mechanisms by which interacts with cognitive function are relatively unknown. Therefore, this paper is part an ongoing study evaluate regional enhancement function. Nicotine-induced changes levels three neurotransmitters, dopamine (DA), serotonin (5-HT), norepinepherine (NE), their metabolites, homovanillic acid (HVA), dihydroxyphenylacetic (DOPAC), 5-hydroxyindoleacetic (5-HIAA), precursor, L-DOPA, were evaluated ventral dorsal hippocampus (VH DH), prefrontal medial temporal cortex (PFC MTC), tegmental area (VTA) using vivo microdialysis awake, freely moving, male Sprague-Dawley rats. animals treated acute (0.5 mg/kg, s.c.) halfway through 300-min experimental period. reuptake blockers, desipramine (100 microM) fluoxetine (30 microM), given increase NE 5-HT so they could be detected. Overall, a nicotine-induced DA was found some areas, potentiated fluoxetine. two HVA DOPAC, increased all throughout experiments, both without inhibitors, indicating rapid metabolism released DA. these metabolites greater than DH, MTC, VTA presence fluoxetine; its metabolite, 5-HIAA, absence Except VTA, similar extent appeared release turnover indicated significant increases metabolites. Furthermore, DA, especially for 150 min following administration; shorter duration. As gas chromatography experiments showed decreased 75% after min, indicate more susceptible lower or NE. In conclusion, administration caused alterations 5-HT, NE, processes.