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Calcium Ion – The Key Player in Cerebral Ischemia

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Role of calcium ion (Ca2+) in the functioning of neurons from their naive 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.

Keywords: Ca2+ channels; Ca2+ ion; ischemia; neuronal damage; neuroprotection

Document Type: Research Article

Publication date: June 1, 2014

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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