Wang Jing, Jackson Michael F, Xie Yu-Feng
Key Laboratory of Orthopedics of Gansu Province, The Second Hospital of Lanzhou University, No. 82 Cui Ying Men, Lanzhou, Gansu 730030, China.
Department of Pharmacology & Therapeutics, University of Manitoba, Canada; Kleysen Institute for Advanced Medicine, University of Manitoba, 710 William Avenue, SR426 Winnipeg, MB, Canada R3E 0Z3.
Neural Plast. 2016;2016:1680905. doi: 10.1155/2016/1680905. Epub 2016 Jan 28.
Synaptic plasticity refers to the ability of neurons to strengthen or weaken synaptic efficacy in response to activity and is the basis for learning and memory. Glial cells communicate with neurons and in this way contribute in part to plasticity in the CNS and to the pathology of Alzheimer's disease (AD), a neurodegenerative disease in which impaired synaptic plasticity is causally implicated. The transient receptor potential melastatin member 2 (TRPM2) channel is a nonselective Ca(2+)-permeable channel expressed in both glial cells (microglia and astrocytes) and neurons. Recent studies indicated that TRPM2 regulates synaptic plasticity as well as the activation of glial cells. TRPM2 also modulates oxidative stress and inflammation through interaction with glial cells. As both oxidative stress and inflammation have been implicated in AD pathology, this suggests a possible contribution of TRPM2 to disease processes. Through modulating the homeostasis of glutathione, TRPM2 is involved in the process of aging which is a risk factor of AD. These results potentially point TRPM2 channel to be involved in AD through glial cells. This review summarizes recent advances in studying the contribution of TRPM2 in health and in AD pathology, with a focus on contributions via glia cells.
突触可塑性是指神经元根据活动情况增强或减弱突触效能的能力，是学习和记忆的基础。神经胶质细胞与神经元进行交流，以此在一定程度上对中枢神经系统的可塑性以及阿尔茨海默病（AD）的病理过程产生影响，AD是一种神经退行性疾病，其中突触可塑性受损被认为与之存在因果关系。瞬时受体电位香草酸亚型2（TRPM2）通道是一种非选择性的钙离子通透通道，在神经胶质细胞（小胶质细胞和星形胶质细胞）和神经元中均有表达。最近的研究表明，TRPM2调节突触可塑性以及神经胶质细胞的激活。TRPM2还通过与神经胶质细胞相互作用来调节氧化应激和炎症。由于氧化应激和炎症都与AD病理过程有关，这表明TRPM2可能对疾病进程有一定作用。通过调节谷胱甘肽的稳态，TRPM2参与了衰老过程，而衰老是AD的一个风险因素。这些结果表明TRPM2通道可能通过神经胶质细胞参与AD。本文综述了TRPM2在健康和AD病理过程中的作用的最新研究进展，重点关注其通过神经胶质细胞所起的作用。
