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Mechanism of anoxic depolarization in the brain
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. Anoxic depolarization is induced by the loss of neuronal membrane permeability. 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. 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 excitotoxins, but high concentrations activate a number of downstream apoptotic and necrotic pathways. This results in neuronal dysfunction and death.
== Neural signal under normal oxygen uptake ==
Neurons function in the central nervous system by generating signals from synapses, and this only works in the proper chemical environment. An electrical signal is mediated by the sodium channels and leaky potassium channels in which intracellular K+ ion concentration is higher than its corresponding extracellular concentration, whereas extracellular concentrations of Na+, Ca2+, and Cl− ions are higher than the corresponding intracellular concentrations. This uneven distribution of ions is maintained by the Na+/K+ ATPase pump which actively pumps Na+ out and K+ into the cell in a ratio of 3:2 per ATP used. A neuron has a resting membrane potential of -70mV due to the leaky potassium channels. As a neuron depolarizes due to Na+ ion influx through the sodium channels, the membrane reaches a threshold potential and then fires an all or none action potential, which either propagates down the axon or passes on to the other neurons via several gap junctions that link them.〔
A chemical signal (synaptic transmission) begins with the action potential that propagates down the axon of so-called presynaptic terminal to trigger Ca2+ influx, which causes the synaptic vesicles to fuse and release neurotransmitters, via exocytosis, to the synaptic cleft.〔 Released neurotransmitters then bind their specific neuroreceptors at the postsynaptic membrane, or activate their specific ligand-gated ion channels, to fire an action potential that can be either excitatory or inhibitory, depending on the nature of the ligand-gated ion channel. Neurotransmitters are removed from the synaptic cleft by either enzymatic degradation or re-uptake by the same presynaptic neuron, via endocytosis or specific neurotransmitter transporters.〔
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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