“School of Cognitive Sciences”
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| Paper IPM / Cognitive Sciences / 12174 |
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Rationale: Nicotine, an active alkaloid of tobacco has an acetylcholine property that alters anxiety-like behaviors in rodents. Moreover, several investigations suggest that the mesolimbic/cortical dopamine systems to be involved in the drugs affecting anxiety. The dopaminergic modulation of acetylcholine synaptic transmission has also been also suggested by different studies. Furthermore, modulation of such behaviors in rodents may be mediated through the dorsal hippocampus. Objectives: In the present study, a possible role of the dorsal hippocampal acetylcholine receptor mechanism in nicotine's influence on anxiogenic-like responses has been investigated. Methods: During test sessions, the hole-board was used to investigate the effects of SCH23390, sulpiride, SKF38393 and quipirole on nicotine response in mice. Results: Intraperitoneal (i.p.) administration of nicotine (0.5 mg/kg) decreased the number of head dips but had no effect on other behaviors. Intra-dorsal hippocampal injections of ineffective doses of SCH23390 (SCH; 0.125 and 0.25 μg/mouse) or sulpiride (SUL; 0.5 and 0.75 μg/mouse) reversed head dips induced by nicotine but did not impact other exploratory behaviors. Furthermore, co-administration of ineffective doses of SKF38393 (SKF; 4 μg/mouse, dorsal hippocampus) or quipirole (QUI; 0.5 μg/mouse) in conjunction with an ineffective dose of nicotine (0.25 mg/kg, i.p.) decreased head dips induced by nicotine, but were otherwise ineffective. Conclusion: These results may indicate a modulatory effect for the dorsal hippocampus dopamine receptors (D1 and D2) on an anxiogenic-like response induced by nicotine.
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