Experimental ischemia induces a persistent depolarization blocked by decreased calcium and NMDA antagonists
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Cellular mechanisms underlying the rapid depolarization caused by oxygen and glucose deprivation in layer III pyramidal cells of the somatosensory cortex
2021, Neuroscience ResearchCitation Excerpt :Even when oxygen and glucose are introduced immediately after generation of the rapid depolarization, the membrane potential reaches approximately 0 mV and cannot repolarize (irreversible depolarization) (Brisson and Andrew, 2012). Consequently, the neurons show no functional recovery (Rader and Lanthorn, 1989). During OGD, the slow depolarization is caused by inhibition of Na+-K+-ATPase activity, which gives rise to an elevation of extracellular K+ concentration, and an accumulation of glutamate.
Neuroprotection for ischemic stroke in the endovascular era: A brief report on the future of intra-arterial therapy
2019, Journal of Clinical NeuroscienceCitation Excerpt :In this brief report, we discuss the pathologic mechanisms of tissue injury in AIS and discuss novel strategies for IA-delivered neuroprotection. Cerebrovascular ischemia halts normal metabolic processes in the brain parenchyma leading to failure of Na+/K+ pumps and abnormal neuronal depolarization, leading to Ca++ influx, which activates intracellular cascades resulting in cellular dysfunction and free-radical generation [3–5]. Pathologic microvascular permeability and disruption of the blood-brain barrier (BBB) ensues, leading to efflux of inflammatory mediators that potentiate BBB disruption, edema formation and activation of matrix metalloproteinases (MMP) [6–11].
Reperfusion Changes After Stroke and Practical Approaches for Neuroprotection
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