Molecular Biology Unit, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego Str., 02-106 Warsaw, Poland.
Int J Mol Sci. 2019 May 9;20(9):2289. doi: 10.3390/ijms20092289.
Neuronal calcium (Ca) influx has long been ascribed mainly to voltage-gated Ca channels and glutamate receptor channels. Recent research has shown that it is also complemented by stromal interaction molecule (STIM) protein-mediated store-operated Ca entry (SOCE). SOCE is described as Ca flow into cells in response to the depletion of endoplasmic reticulum Ca stores. The present review summarizes recent studies that indicate a relationship between neuronal SOCE that is mediated by STIM1 and STIM2 proteins and glutamate receptors under both physiological and pathological conditions, such as neurodegenerative disorders. We present evidence that the dysregulation of neuronal SOCE and glutamate receptor activity are hallmarks of acute neurodegenerative diseases (e.g., traumatic brain injury and cerebral ischemia) and chronic neurodegenerative diseases (e.g., Alzheimer's disease and Huntington's disease). Emerging evidence indicates a role for STIM proteins and glutamate receptors in neuronal physiology and pathology, making them potential therapeutic targets.
神经元钙 (Ca) 内流长期以来主要归因于电压门控 Ca 通道和谷氨酸受体通道。最近的研究表明，它还通过基质相互作用分子 (STIM) 蛋白介导的储存操作 Ca 内流 (SOCE) 得到补充。SOCE 被描述为细胞内 Ca 流响应内质网 Ca 储存耗尽的反应。本综述总结了最近的研究，这些研究表明，在生理和病理条件下，由 STIM1 和 STIM2 蛋白介导的神经元 SOCE 与谷氨酸受体之间存在关系，如神经退行性疾病。我们提供的证据表明，神经元 SOCE 和谷氨酸受体活性的失调是急性神经退行性疾病（例如，创伤性脑损伤和脑缺血）和慢性神经退行性疾病（例如，阿尔茨海默病和亨廷顿病）的标志。新出现的证据表明 STIM 蛋白和谷氨酸受体在神经元生理学和病理学中的作用，使它们成为潜在的治疗靶点。
