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首页> 外文期刊>Life sciences >Nicotine improves ethanol-induced memory impairment: The role of dorsal hippocampal NMDA receptors
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Nicotine improves ethanol-induced memory impairment: The role of dorsal hippocampal NMDA receptors

机译：尼古丁改善乙醇诱发的记忆障碍：背海马NMDA受体的作用

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Aims: The current study was undertaken to determine the role of dorsal hippocampal N-methyl-D-aspartate (NMDA) receptors in nicotine's effect on impairment of memory by ethanol.Main methods: Adult male mice were cannulated in the CA1 regions of dorsal hippocampi and trained on a passive avoidance learning task for memory assessment.Key findings: We found that pre-training intraperitoneal (i.p.) administration of ethanol (0.5 and 1 g/kg) decreased memory retrieval when tested 24 h later. Pre-test administration of ethanol reversed the decrease in inhibitory avoidance response induced by pre-training ethanol. Similar to ethanol, pre-test administration of nicotine (0.125-0.75 mg/kg, s.c.) prevented impairment of memory by pre-training ethanol. In the animals that received ethanol (1 g/kg, i.p) before training and tested following intra-CAl administration of different doses of NMDA (0.0005-0.005 ug/mouse), no significant change was observed in the retrieval latencies. Co-administration of the same doses of NMDA with an ineffective dose of nicotine (0.125 mg/kg, s.c.) significantly improved the memory retrieval and mimicked the effects of pre-test administration of a higher dose of nicotine. Pre-test intra-CAl microinjection of MK-801 (0.25-1 ug/mouse), which had no effect alone, in combination with an effective dose of nicotine (0.75 mg/kg, s.c.) prevented the improving effect of nicotine on memory impaired by pre-training ethanol. Moreover, intra-CAl microinjection of MK-801 reversed the NMDA-induced potentiation of the nicotine response.Significance: The results suggest the importance of NMDA glutamate system(s) in the CA1 regions of dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia.
机译：目的：本研究旨在确定海马背侧海马N-甲基-D-天冬氨酸（NMDA）受体在尼古丁对乙醇引起的记忆障碍的影响中的作用。主要方法：成年雄性小鼠在海马背侧CA1区插管。关键发现：我们发现在训练24小时后进行腹膜内（ip）乙醇（0.5和1 g / kg）腹腔内（ip）给药会减少记忆恢复。乙醇的预测试给药逆转了由乙醇预训练引起的抑制回避反应的减少。与乙醇相似，尼古丁的预试验给药（0.125-0.75 mg / kg，皮下注射）可通过预训练乙醇来防止记忆力受损。在训练前接受乙醇（1 g / kg，腹腔内）的动物中，以及在CAA内施用不同剂量的NMDA（0.0005-0.005 ug /小鼠）后进行测试的动物中，恢复潜伏期未观察到明显变化。相同剂量的NMDA与无效剂量的尼古丁（0.125 mg / kg，s.c.）共同给药显着改善了记忆恢复，并模仿了高剂量尼古丁的试验前给药效果。单独进行测试的MK-801（0.25-1 ug /小鼠）的CAl预测试内显微注射与有效剂量的尼古丁（0.75 mg / kg，sc）结合使用无法阻止尼古丁改善记忆力预先训练乙醇会受损。此外，CA1内显微注射MK-801逆转了NMDA诱导的尼古丁应答增强作用。意义：结果表明，NMDA谷氨酸系统在背侧海马CA1区对改善尼古丁对尼古丁的影响具有重要意义乙醇引起的健忘症。

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