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大鼠端脑衰老过程中PSA-NCAM表达的差异演变。

Differential evolution of PSA-NCAM expression during aging of the rat telencephalon.

作者信息

Varea Emilio, Castillo-Gómez Esther, Gómez-Climent María Angeles, Guirado Ramón, Blasco-Ibáñez José Miguel, Crespo Carlos, Martínez-Guijarro Francisco José, Nácher Juan

机构信息

Neurobiology Unit and Program in Basic and Applied Neurosciences, Cell Biology Dpt., Universitat de València, Dr. Moliner 50, Burjassot 46100, Spain.

出版信息

Neurobiol Aging. 2009 May;30(5):808-18. doi: 10.1016/j.neurobiolaging.2007.08.016. Epub 2007 Sep 29.

Abstract

Changes in the ability of neuronal networks to undergo structural remodeling may be involved in the age-associated cognitive decline. The polysialylated form of the neural cell adhesion molecule (PSA-NCAM) declines dramatically during postnatal development, but persists in several regions of the young-adult rat telencephalon, where it participates, through its anti-adhesive properties, in neuronal structural plasticity. However, PSA-NCAM expression during aging has only been studied in the dentate gyrus and the piriform cortex layer II, where it is strongly downregulated in adult (middle-aged) individuals. Using immunohistochemistry, we have observed that in most of the telencephalic areas studied the number of PSA-NCAM expressing cells and the intensity of PSA-NCAM expression in the neuropil remains stable during aging. Old rats only show decreases in the number of PSA-NCAM expressing cells in the lateral amygdala and retrosplenial cortex, and in neuropil expression of stratum lucidum. Given the role of PSA-NCAM in neuronal plasticity, the present results indicate that, even during aging, many regions of the CNS may display neurite, spine or synaptic remodeling.

摘要

神经网络进行结构重塑能力的变化可能与年龄相关的认知衰退有关。神经细胞黏附分子的多唾液酸化形式(PSA-NCAM)在出生后发育过程中急剧下降,但在成年大鼠端脑的几个区域持续存在,它通过其抗黏附特性参与神经元结构可塑性。然而,衰老过程中PSA-NCAM的表达仅在齿状回和梨状皮层II层进行了研究,在成年(中年)个体中它在这些区域被强烈下调。使用免疫组织化学方法,我们观察到在大多数研究的端脑区域,衰老过程中表达PSA-NCAM的细胞数量以及神经毡中PSA-NCAM表达的强度保持稳定。老年大鼠仅在外侧杏仁核和脾后皮质中表达PSA-NCAM的细胞数量以及透明层的神经毡表达出现减少。鉴于PSA-NCAM在神经元可塑性中的作用,目前的结果表明,即使在衰老过程中,中枢神经系统的许多区域仍可能表现出神经突、棘或突触重塑。

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