Global InformationAnoxic depolarization in the brain information
 | This article may be too technical for most readers to understand. (November 2013) |
Anoxic depolarization is a progressive and uncontrollable depolarization of neurons during stroke or brain ischemia in which there is an inadequate supply of blood to the brain.[1] Anoxic depolarization is induced by the loss of neuronal selective membrane permeability and the ion gradients across the membrane that are needed to support neuronal activity. Normally, the Na+/K+-ATPase pump maintains the transmembrane gradients of K+ and Na+ ions, but with anoxic brain injury, the supply of energy to drive this pump is lost.[2] The hallmarks of anoxic depolarization are increased concentrations of extracellular K+ ions, intracellular Na+ and Ca2+ ions, and extracellular glutamate and aspartate. Glutamate and aspartate are normally present as the brain's primary excitatory neurotransmitters, but high concentrations activate a number of downstream apoptotic and necrotic pathways. This results in neuronal dysfunction and brain death.[3]
- ^ Weilinger NL, Maslieieva V, Bialecki J, Sridharan SS, Tang PL, Thompson RJ (2013). "Ionotropic receptors and ion channels in ischemic neuronal death and dysfunction". Acta Pharmacol Sin. 34 (1): 39–48. doi:10.1038/aps.2012.95. PMC 4086487. PMID 22864302.
- ^ Stys, P. (1998). "Anoxic and ischemic injury of myelinated axons in CNS white matter: from Mechanistic Concepts to Therapeutics". Journal of Cerebral Blood Flow and Metabolism. 18 (1): 2–25. doi:10.1097/00004647-199801000-00002. PMID 9428302.
- ^ Nilsson, G.; Lutz, P (2004). "Anoxia tolerant brains". Journal of Cerebral Blood Flow and Metabolism. 24 (5): 475–486. doi:10.1097/00004647-200405000-00001. PMID 15129179.