عنوان مقاله [English]
نویسندگان [English]چکیده [English]
Ethanol and nicotine produce some effects via activation of mesocorticolimbic dopaminergic pathway which projects from the ventral tegmental area to the nucleus accumbens and hippocampus. Dopamine D2 receptors have been detected in dorsal hippocampus, which is a key brain region that influences learning and memory. In the present study, influence of dopamine D2 receptors of dorsal hippocampus in nicotineandrsquo;s effect on ethanol-induced amnesia was investigated. In this experimental study 255 adult male NMRI mice were used (24 group). The animals anaesthetized and cannulae implanted bilaterally in the CA1 regions of the dorsal hippocampus using stereotaxic method. Seven days after recovery from surgery, the behavioral testing was started in inhibitory avoidance task. In this study ethanol, nicotine and sulpiride (D2 receptor agonist) were used. The Kruskalandndash;Wallis nonparametric one-way analysis of variance (ANOVA) followed by a two-tailed Mannandndash;Whitneyand#39;s U-test, were used for analysis of the data. Differences with P andlt; 0.05 between experimental groups at each point were considered statistically significant. Pre-training or pre-test injection of ethanol induced amnesia (Pandlt;0.001). Pre-test administration of ethanol or nicotine restored amnesia ethanol (Pandlt;0.001). Pre-test intra-CA1 injection of sulpirideblocks the nicotine reversal effect on ethanol amnesia (Pandlt;0.001).On the other hand, pre-test injection of nicotine or sulpiride has no effect on memory by itself (Pandgt;0.05). Our results in this study indicated that the blockage of dopamine d1 receptors of dorsal hippocampus decreases nicotine-induced restoration of ethanol amnesia.