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多奈哌齐给药不能挽救甘丙肽诱导的空间学习缺陷。

Administration of donepezil does not rescue galanin-induced spatial learning deficits.

机构信息

Behavioral Neuroscience Laboratory, University of Nevada , Las Vegas, Las Vegas, Nevada 89154, USA.

出版信息

Int J Neurosci. 2012 Dec;122(12):742-7. doi: 10.3109/00207454.2012.721411. Epub 2012 Oct 11.

Abstract

The neuropeptide galanin inhibits the evoked release of several neurotransmitters including acetylcholine and modulates adenylate cyclase (AC) activity. Galanin has also been established to impair various forms of learning and memory in rodents. However, whether galanin produces learning deficits by inhibiting cholinergic activity or decreasing AC function has not been clearly established. The current study investigated if donepezil, an acetylcholinesterase inhibitor utilized in Alzheimer's disease, could rescue galanin-induced Morris water task deficits in rats. The results demonstrated that donepezil did not alter the previously established deficits induced by galanin. These findings suggest that galanin-mediated spatial learning deficits may be unrelated to its modulation of the cholinergic system.

摘要

神经肽甘丙肽抑制包括乙酰胆碱在内的几种神经递质的诱发释放,并调节腺苷酸环化酶 (AC) 的活性。甘丙肽已被证实可损害啮齿动物的各种形式的学习和记忆。然而,甘丙肽是否通过抑制胆碱能活性或降低 AC 功能产生学习缺陷尚不清楚。本研究探讨了多奈哌齐(一种用于治疗阿尔茨海默病的乙酰胆碱酯酶抑制剂)是否可以挽救甘丙肽诱导的大鼠 Morris 水迷宫任务缺陷。结果表明,多奈哌齐并未改变甘丙肽先前引起的缺陷。这些发现表明,甘丙肽介导的空间学习缺陷可能与其对胆碱能系统的调节无关。

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