Modes of Calcium Regulation in Ischemic Neuron

Abstract

Calcium (Ca 2?) dysregulation is a major catalytic event. Ca 2? dysregulation leads to neuronal cell death and brain damage result in cerebral ischemia. Neurons are unable in maintaining calcium homeostasis. Ca 2? homeostasis imbalance results in increased calcium influx and impaired calcium extrusion across the plasma membrane. Ca 2? dysregulation is mediated by different cellular and biochemical mechanism, which leads to neuronal loss resulting stroke/cerebral ischemia. A better understanding of the Ca 2? dysregulation might help in the development of new treatments in order to reduce ischemic brain injury. An optimal concentration of Ca 2? does not lead to neurotoxicity in the ischemic neuron. Intracellular Ca 2? 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 Ca 2? influx to neurons, involvement of intracellular Ca 2? stores and Ca 2? buffers, spatial and temporal relations between ischemia-induced increases in intracellular Ca 2? 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 Ca 2? influx pathways involve in ischemic neuron and how ischemic neuron attempts to counterbalance this calcium overload.

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

“…The ways of calcium entering neurons following cerebral ischemia include glutamate receptors; voltage-dependent calcium channel; transient receptor potential channels; acid-sensing ion channels; sodium-calcium exchanger operating in entry mode; inward excitotoxic injury current calcium permeable channels; mitochondria and endoplasmic reticulum calcium release, etc. And the pathways of calcium exit into neurons include Ca 2+ -ATPase pump; Na + -Ca 2+ exchanger operating in exit mode, etc ( Singh et al, 2019 ).…”

In Vitro Evaluation of the Neuroprotective Effect of Panax notoginseng Saponins by Activating the EGFR/PI3K/AKT Pathway

“…e main cause of death and disability after ischemic stroke is caused by decreased neuroprotection and neuroregeneration in the ischemic area [17]. Free radicals and Evidence-Based Complementary and Alternative Medicine calcium overload are widely studied mechanisms in the pathological processes of ischemic damage, especially at the stage of ischemia reperfusion [18][19][20]. e brain generates more free radicals than any other organs, resulting in free radical damage of brain tissue [21].…”

Mechanism of Endoplasmic Reticulum Stress in Cerebral Ischemia

“…The interruption of energy supply due to oxygen and glucose deprivation following cerebral ischemia can give rise to the deficiency of ATP ion channels and sustained neuronal depolarization. Under the state of abnormal electrochemical gradient and cells depolarization, over-opening voltage-dependent Ca 2+ channels (VDCCs) and unintentional release of the neurotoxic excitatory neurotransmitter glutamate which activates N-methyl-d-aspartate receptors (NMDARs) leading to incremental intracellular Ca 2+ concentration and excitotoxicity ( Szydlowska and Tymianski, 2010 ; Singh et al, 2019 ). Neurons and oligodendrocytes are intensively sensitive to NMDA mediated excitotoxicity, which is responsible for their fatal death at the early stage.…”