Early effects of hypoxia on brain cell function.

摘要: This article reviews the changes in neuronal function produced by oxygen lack, especially as observed hippocampal slices vitro. An early cessation of electrical activity ("firing"), caused a K+ conductance-mediated hyperpolarization and disappearance excitatory synaptic potentials (EPSPs), can be seen protective mechanism that prevents cellular damage resulting from severe mismatch between energy needs supplies. These are triggered such hypoxia-induced signals rise cytoplasmic free calcium, fall adenosine triphosphate (ATP), extracellular accumulation (produced ATP breakdown). Upon reoxygenation, suppression neuronal/synaptic is quite reversible, long hypoxic nerve cells have an adequate supply glucose. But if sufficient cannot obtained anerobic glycolysis to maintain essential Na-K pump protein synthesis, long-term cell functi on survival compromised. Thus, when both glucose deficient, strokes, mechanisms prevent lethal effects excessive Ca2+ influx.