Regulation of extracellular potassium concentration in epileptogenesis.
Characteristic elevations in the brain's extracellular potassium concentration [K+]0 occur during focal epileptogenesis. These changes have particular spatial and temporal profiles that are different in hippocampus and neocortex, and in mature and immature animals. Increases in [K+]0 cannot be the sole explanation for regional variations in seizure susceptibility, interictal-ictal transitions, or termination of ictal episodes. Excess [K+]0 is cleared primarily by passive diffusion with a small amount taken up into cells and blood vessels. Cortical neuroglia have sensitivities to changes in [K+]0 similar to that observed in glial cells in invertebrates and amphibia. However, discrepancies in the expected relationship between [K+]o and glial membrane potential Vm suggest either a heterogeneous population of glial cell types and/or the presence of a glial syncytium which acts as a spatial buffer to increases in [K+]0.
D000818:Animals; D001693:Biological Transport, Active; D001921:Brain / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism; D004058:Diffusion; D004828:Epilepsies, Partial / Q000378:metabolism*; D005110:Extracellular Space / Q000378:metabolism*; D005911:Gliosis / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D012640:Seizures / Q000378:metabolism*
D011188:Potassium