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mdx小鼠的空间学习能力和海马体长期增强效应未受损。

Spatial learning and hippocampal long-term potentiation are not impaired in mdx mice.

作者信息

Sesay A K, Errington M L, Levita L, Bliss T V

机构信息

Division of Neurophysiology, National Institute for Medical Research, London, UK.

出版信息

Neurosci Lett. 1996 Jun 28;211(3):207-10. doi: 10.1016/0304-3940(96)12747-6.

DOI:10.1016/0304-3940(96)12747-6
PMID:8817577
Abstract

Moderate non-progressive cognitive impairment is a consistent feature of Duchenne muscular dystrophy (DMD), although few central nervous system abnormalities have yet been identified. A model for DMD is provided by the mdx mouse which fails to produce full length dystrophin in muscle and brain. In this study we have compared performances in a hippocampal-dependent spatial learning task, the Morris water maze, in mdx mice and in age-matched normal (C57BL/10) mice. There was no difference in acquisition rates or in retention between the two groups. We also found no difference in the magnitude of long-term potentiation (LTP) between the two groups, either in the dentate gyrus or in area CA. These experiments demonstrate that neither spatial learning nor hippocampal synaptic plasticity are significantly affected by the lack of full-length dystrophin.

摘要

中度非进行性认知障碍是杜氏肌营养不良症(DMD)的一个持续特征,尽管目前尚未发现中枢神经系统有明显异常。mdx小鼠为DMD提供了一个模型,该小鼠在肌肉和大脑中无法产生全长抗肌萎缩蛋白。在本研究中,我们比较了mdx小鼠和年龄匹配的正常(C57BL/10)小鼠在依赖海马体的空间学习任务——莫里斯水迷宫中的表现。两组之间在习得率或记忆保持方面没有差异。我们还发现,两组在齿状回或CA区的长时程增强(LTP)幅度上也没有差异。这些实验表明,缺乏全长抗肌萎缩蛋白并不会显著影响空间学习或海马体突触可塑性。

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