Kumar V S Suvanish, Gopalakrishnan A, Naziroğlu M, Rajanikant G K
School of Biotechnology, Coordinator, DBT -Centre for Bioinformatics, National Institute of Technology Calicut, Calicut 673601, India.
Curr Med Chem. 2014;21(18):2065-75. doi: 10.2174/0929867321666131228204246.
Role of calcium ion (Ca2+) in the functioning of neurons from their naïve state to mature state is of vital importance. It controls functions such as neuronal functioning, neuronal ATP production, central nervous system migration and many others. Failure in Ca2+ homeostasis mechanisms and the resulting cellular Ca2+ ion load initiates a cascade of reactions involving various cytosolic enzymes and proteins. This total mechanism leads to the neuronal death. The ability of neurons to resist such death mechanisms fails as a result of extensive cell death signaling cascade reactions and later brings brain damage. The role of neuronal endoplasmic reticulum and protein channels like CaVs, TRP channels, and NMDAR as the mediators of cell damage and death has been evaluated in the studies related to cerebral ischemia. Here, we portray Ca2+ ion as one of the role players in neuronal death and cerebral damage following ischemia. The role of Ca2+ in neuronal functioning, its regulatory mechanisms and the failure of homeostatic mechanisms are discussed in detail.
钙离子（Ca2+）在神经元从幼稚状态到成熟状态的功能发挥中起着至关重要的作用。它控制着诸如神经元功能、神经元ATP生成、中枢神经系统迁移等多种功能。Ca2+稳态机制的失效以及由此产生的细胞内Ca2+离子负荷会引发一系列涉及各种胞质酶和蛋白质的反应。这一整体机制会导致神经元死亡。由于广泛的细胞死亡信号级联反应，神经元抵抗这种死亡机制的能力会失效，进而导致脑损伤。在与脑缺血相关的研究中，已经评估了神经元内质网以及诸如CaV、瞬时受体电位（TRP）通道和N-甲基-D-天冬氨酸受体（NMDAR）等蛋白质通道作为细胞损伤和死亡介质的作用。在此，我们将Ca2+离子描述为缺血后神经元死亡和脑损伤的关键因素之一。本文将详细讨论Ca2+在神经元功能中的作用、其调节机制以及稳态机制的失效。
