Ion and membrane changes in the brain during anoxia.
Anoxia has two main effects on the brain, a rapid, reversible loss of function and permanent damage when the period of anoxia exceeds a critical length of time. The initial loss of function is related to a K+-conductance increase of the nerve membrane, leading to reduction of membrane resistance and hyperpolarization. After a few minutes, a non-selective increase of membrane permeability mediates rapid transfer of ions between the intra- and extracellular spaces. The subsequent rise of intracellular Ca2+ concentration may be responsible for the nerve cell death.
D000136:Acid-Base Equilibrium; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D004569:Electroencephalography; D006801:Humans; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007473:Ion Channels / Q000502:physiology*; D007477:Ions / Q000378:metabolism*; D008564:Membrane Potentials; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D001786:Blood Glucose; D007473:Ion Channels; D007477:Ions; D018377:Neurotransmitter Agents; D000255:Adenosine Triphosphate; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium