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关于谷氨酸稳态改变如何可能导致中枢神经系统脱髓鞘疾病。

On how altered glutamate homeostasis may contribute to demyelinating diseases of the CNS.

作者信息

Matute C, Domercq M, Fogarty D J, Pascual de Zulueta M, Sánchez-Gómez M V

机构信息

Departamento de Neurociencias Universidad del País Vasco, Vizcaya, Spain.

出版信息

Adv Exp Med Biol. 1999;468:97-107.

Abstract

Glial cells communicate reciprocally with neurons in multiple ways, both in synaptic and non-synaptic regions of the central nervous system. In the latter, neuron to glial and glial to glial signals can be mediated by neurotransmitters. Here, we review the presence and some of the functional properties of glutamate transporters and receptors in oligodendrocytes. In addition, we present data illustrating that alterations in glutamate homeostasis can be excitotoxic to oligodendroglia and that the tissue lesions caused by overactivation of glutamate receptors resemble those observed in demyelinating diseases such as multiple sclerosis. Overall, this information indicates that aberrant glutamate signaling may contribute to the development of some white matter pathologies.

摘要

神经胶质细胞通过多种方式与神经元相互交流,在中枢神经系统的突触和非突触区域均是如此。在非突触区域,神经元与神经胶质细胞以及神经胶质细胞与神经胶质细胞之间的信号可由神经递质介导。在此,我们综述少突胶质细胞中谷氨酸转运体和受体的存在情况及其一些功能特性。此外,我们还展示了数据,表明谷氨酸稳态的改变可能对少突胶质细胞具有兴奋性毒性,且谷氨酸受体过度激活所导致的组织损伤类似于在多发性硬化症等脱髓鞘疾病中观察到的损伤。总体而言,这些信息表明异常的谷氨酸信号传导可能促成某些白质病变的发展。

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