Vijaya Nath Mishra

Calcium (Ca²⁺) dysregulation is a major catalytic event. Ca²⁺ dysregulation leads to neuronal cell death and brain damage result in cerebral ischemia. Neurons are unable in maintaining calcium homeostasis. Ca²⁺ homeostasis imbalance results in increased calcium influx and impaired calcium extrusion across the plasma membrane. Ca²⁺ dysregulation is mediated by different cellular and biochemical mechanism, which leads to neuronal loss resulting stroke/cerebral ischemia. A better understanding of the Ca²⁺ dysregulation might help in the development of new treatments in order to reduce ischemic brain injury. An optimal concentration of Ca²⁺ does not lead to neurotoxicity in the ischemic neuron. Intracellular Ca²⁺ act as a trigger for acute neurotoxicity and this cause induction of long-lasting processes leading to necrotic and/or apoptotic post-ischemic delayed neuronal death or of compensatory, neuroprotective mechanisms has increased considerably. Moreover, routes of ischemic Ca²⁺ influx to neurons, involvement of intracellular Ca²⁺ stores and Ca²⁺ buffers, spatial and temporal relations between ischemia-induced increases in intracellular Ca²⁺ concentration and neurotoxicity will further increase our understanding about underlying mechanism and they can act as a target for the development of drugs. Here, in our article we are trying to provide a brief overview of various Ca²⁺ influx pathways involve in ischemic neuron and how ischemic neuron attempts to counterbalance this calcium overload.