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一种新型的海马体认知缺陷、缓慢神经退行性变和神经再生的动物模型。

A novel animal model of hippocampal cognitive deficits, slow neurodegeneration, and neuroregeneration.

作者信息

Spanswick Simon C, Lehmann Hugo, Sutherland Robert J

机构信息

Department of Psychology, University of Calgary, Calgary, AB, Canada.

出版信息

J Biomed Biotechnol. 2011;2011:527201. doi: 10.1155/2011/527201. Epub 2011 Mar 15.

Abstract

Long-term adrenalectomy (ADX) results in an extensive and specific loss of dentate gyrus granule cells in the hippocampus of adult rats. This loss of granule cells extends over a period of weeks to months and ultimately results in cognitive deficits revealed in a number of tasks that depend on intact hippocampal function. The gradual nature of ADX-induced cell death and the ensuing deficits in cognition resemble in some important respects a variety of pathological conditions in humans. Here, we characterize behavioural and cellular processes, including adult neurogenesis, in the rat ADX model. We also provide experimental evidence for a neurogenic treatment strategy by which the lost hippocampal cells may be replaced, with the goal of functional recovery in mind.

摘要

长期肾上腺切除术(ADX)会导致成年大鼠海马齿状回颗粒细胞广泛且特异性地丧失。这种颗粒细胞的丧失会持续数周甚至数月,最终导致在一些依赖完整海马功能的任务中出现认知缺陷。ADX诱导的细胞死亡的渐进性以及随之而来的认知缺陷在某些重要方面类似于人类的多种病理状况。在此,我们对大鼠ADX模型中的行为和细胞过程进行了表征,包括成年神经发生。我们还为一种神经源性治疗策略提供了实验证据,该策略旨在替换丢失的海马细胞,以期实现功能恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6012/3085481/516fce68a2b7/JBB2011-527201.001.jpg

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