Elsevier

Neuroscience Letters

Volume 99, Issues 1–2, 24 April 1989, Pages 125-130
Neuroscience Letters

Experimental ischemia induces a persistent depolarization blocked by decreased calcium and NMDA antagonists

https://doi.org/10.1016/0304-3940(89)90276-0Get rights and content

Abstract

Early physiological events induced by hypoxia plus low d-glucose were investigated by intracellular recording in the rat hippocampal slice. A rapid intracellular depolarization corresponded to the extracellularly recorded anoxic depolarization. This intracellular depolarization consisted of two pharmacologically distinct components, an initial depolarization and a persistent depolarization. The persistent phase of depolarization was selectively blocked by lowering calcium and raising magnesium and by N-methyl-d-aspartate (NMDA) antagonists. This persistent depolarization can account for the long-term synaptic failure seen following experimental ischemia in vitro.

Cited by (89)

  • Cellular mechanisms underlying the rapid depolarization caused by oxygen and glucose deprivation in layer III pyramidal cells of the somatosensory cortex

    2021, Neuroscience Research
    Citation 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 Neuroscience
    Citation 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].

  • Network Control Mechanisms-Cellular Milieu

    2014, Neuronal Networks in Brain Function, CNS Disorders, and Therapeutics
View all citing articles on Scopus
View full text