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Potassium Spatial Buffering is a mechanism for the regulation of extracellular potassium concentration by astrocytes. Other mechanisms for astrocytic potassium clearance are carrier-operated or channel-operated potassium chloride uptake.〔Walz W (2000): Role of astrocytes in the clearance of excess extracellular potassium. Neurochemistry International〕 The depolarization of neurons tends to raise potassium concentration in the extracellular fluid. If a significant rise occurs, it will interfere with neuronal signaling by depolarizing neurons. Astrocytes have large numbers of potassium ion channels facilitating removal of potassium ions from the extracellular fluid. They are taken up at one region of the astrocyte and then distributed throughout the cytoplasm of the cell, and further to its neighbors via gap junctions. This keeps extracellular potassium at levels that prevent interference with normal propagation of an action potential. ==Potassium Spatial Buffering== Glial cells, once believed to have a passive role in CNS, are active regulators of numerous functions in the brain, including clearance of the neurotransmitter from the synapses, guidance during neuronal migration, control of neuronal synaptic transmission, and maintaining ideal ionic environment for active communications between neurons in central nervous system.〔Kozoriz, M. G., D. C. Bates, et al. (2006). "Passing potassium with and without gap junctions." Journal of Neuroscience 26(31): 8023-8024.〕 Neurons are surrounded by extracellular fluid rich in sodium ions and poor in potassium ions. The concentrations of these ions are reversed inside the cells. Due to the difference in concentration, there is a chemical gradient across the cell membrane, which leads to sodium influx and potassium efflux. When the action potential takes place, a considerable change in extracellular potassium concentration occurs due to the limited volume of the CNS extracellular space. The change in potassium concentration in extracellular space impacts variety of neuronal processes, such as maintenance of membrane potential, activation and inactivation of voltage gated channels, synaptic transmission, and electrogenic transport of neurotransmitter. Change of extracellular potassium concentration of from 3mM can affect neural activity. Therefore, there are diverse cellular mechanisms for tight control of potassium ions, the most widely accepted mechanisms being K+ spatial buffering mechanism. Orkand and his colleagues who first theorized spatial buffering stated “if a Glial cell becomes depolarized by K+ that has accumulated in the clefts, the resulting current carries K+ inward in the high () region and out again, through electrically coupled Glial cells in low () regions” In the model presented by Orkand and his colleagues, glial cells intake and traverse potassium ions from region of high concentrations to region of low concentration maintaining potassium concentration to be low in extracellular space. Glial cells are well suited for transportation of potassium ions since it has unusually high permeability to potassium ions and traverse long distance by its elongated shape or by being coupled to one another.〔Chen, K. C. and C. Nicholson (2000). "Spatial buffering of potassium ions in brain extracellular space." Biophysical Journal 78(6): 2776-2797.〕〔Xiong, Z. Q. and F. L. Stringer (2000). "Sodium pump activity, not glial spatial buffering, clears potassium after epileptiform activity induced in the dentate gyrus." Journal of Neurophysiology 83(3): 1443-1451.〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Potassium spatial buffering」の詳細全文を読む スポンサード リンク
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