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• W1971597564 abstract "Extracellular [K+] can range within 2.5–3.5 mM under normal conditions to 50–80 mM under ischemic and spreading depression events. Sustained exposure to elevated [K+]o has been shown to cause significant neuronal death even under conditions of abundant glucose supply. Astrocytes are well equipped to buffer this initial insult of elevated [K] through extensive gap junctional coupling, Na+/K+ pump activity (with associated glycogen and glycolytic potential), and endfoot siphoning capability. Their abundant energy availability and alkalinizing mechanisms help sustain Na+/K+ ATPase activity under ischemic conditions. Furthermore, passive K+ uptake mechanisms and water flux mediated through aquaporin-4 channels in endfoot processes are important energy-independent mechanisms. Unfortunately, as the length of ischemic episode is prolonged, these mechanisms increase to a point where they begin to have repercussions on other important cellular functions. Alkalinizing mechanisms induce an elevation of [Na+]i, increasing the energy demand of Na+/K+ ATPase and leading to eventual detrimental reversal of the Na+/glutamate− cotransporter and excitotoxic damage. Prolonged ischemia also results in cell swelling and activates volume regulatory processes that release excessive excitatory amino acids, further exacerbating excitotoxic injury. In the days following ischemic injury, reactive astrocytes demonstrate increased cell size and process thickness, leading to improved spatial buffering capacity in regions outside the lesion core where there is better neuronal survival. There is a substantial heterogeneity among reactive astrocytes, with some close to the lesion showing decreased buffering capacity. However, it appears that both Na+/K+ ATPase activity (along with energy production processes) as well as passive K+ uptake mechanisms are upregulated in gliotic tissue outside the lesion to enhance the above-mentioned homeostatic mechanisms. © 2005 Wiley-Liss, Inc." @default.
• W1971597564 created "2016-06-24" @default.
• W1971597564 creator A5017992417 @default.
• W1971597564 creator A5042035828 @default.
• W1971597564 creator A5083634411 @default.
• W1971597564 date "2005-04-21" @default.
• W1971597564 modified "2023-09-23" @default.
• W1971597564 title "Potassium homeostasis in the ischemic brain" @default.
• W1971597564 cites W1495656315 @default.
• W1971597564 cites W1497027759 @default.
• W1971597564 cites W1539041562 @default.
• W1971597564 cites W1575013471 @default.
• W1971597564 cites W1593228500 @default.
• W1971597564 cites W1593655973 @default.
• W1971597564 cites W1627210966 @default.
• W1971597564 cites W1928529925 @default.
• W1971597564 cites W1936849452 @default.
• W1971597564 cites W1942797206 @default.
• W1971597564 cites W1965766460 @default.
• W1971597564 cites W1967001670 @default.
• W1971597564 cites W1971502696 @default.
• W1971597564 cites W1972599392 @default.
• W1971597564 cites W1973847443 @default.
• W1971597564 cites W1974594239 @default.
• W1971597564 cites W1974761603 @default.
• W1971597564 cites W1983197885 @default.
• W1971597564 cites W1990900542 @default.
• W1971597564 cites W1992231858 @default.
• W1971597564 cites W1993054081 @default.
• W1971597564 cites W1994416969 @default.
• W1971597564 cites W1994446024 @default.
• W1971597564 cites W1995916371 @default.
• W1971597564 cites W2001849349 @default.
• W1971597564 cites W2007654857 @default.
• W1971597564 cites W2011706581 @default.
• W1971597564 cites W2014151097 @default.
• W1971597564 cites W2014493691 @default.
• W1971597564 cites W2017168652 @default.
• W1971597564 cites W2020173902 @default.
• W1971597564 cites W2020753680 @default.
• W1971597564 cites W2021733097 @default.
• W1971597564 cites W2023550610 @default.
• W1971597564 cites W2027609915 @default.
• W1971597564 cites W2028072707 @default.
• W1971597564 cites W2028977278 @default.
• W1971597564 cites W2031135416 @default.
• W1971597564 cites W2035371282 @default.
• W1971597564 cites W2036305842 @default.
• W1971597564 cites W2039824205 @default.
• W1971597564 cites W2047687479 @default.
• W1971597564 cites W2049554245 @default.
• W1971597564 cites W2052070303 @default.
• W1971597564 cites W2052350415 @default.
• W1971597564 cites W2054467746 @default.
• W1971597564 cites W2055168645 @default.
• W1971597564 cites W2055852420 @default.
• W1971597564 cites W2055891615 @default.
• W1971597564 cites W2056251473 @default.
• W1971597564 cites W2056768860 @default.
• W1971597564 cites W2060338837 @default.
• W1971597564 cites W2065024312 @default.
• W1971597564 cites W2066285544 @default.
• W1971597564 cites W2066840018 @default.
• W1971597564 cites W2067018626 @default.
• W1971597564 cites W2071661190 @default.
• W1971597564 cites W2072003572 @default.
• W1971597564 cites W2080706601 @default.
• W1971597564 cites W2085921954 @default.
• W1971597564 cites W2087588464 @default.
• W1971597564 cites W2089450477 @default.
• W1971597564 cites W2090972175 @default.
• W1971597564 cites W2092046923 @default.
• W1971597564 cites W2092824003 @default.
• W1971597564 cites W2097738779 @default.
• W1971597564 cites W2097833693 @default.
• W1971597564 cites W2098436218 @default.
• W1971597564 cites W2103230981 @default.
• W1971597564 cites W2109584356 @default.
• W1971597564 cites W2112462409 @default.
• W1971597564 cites W2114958991 @default.
• W1971597564 cites W2115217673 @default.
• W1971597564 cites W2116447221 @default.
• W1971597564 cites W2130004067 @default.
• W1971597564 cites W2134046709 @default.
• W1971597564 cites W2141610399 @default.
• W1971597564 cites W2143647842 @default.
• W1971597564 cites W2150454711 @default.
• W1971597564 cites W2151305004 @default.
• W1971597564 cites W2158738489 @default.
• W1971597564 cites W2162889119 @default.
• W1971597564 cites W2163161737 @default.
• W1971597564 cites W2164554425 @default.
• W1971597564 cites W2169334356 @default.
• W1971597564 cites W2169759057 @default.
• W1971597564 cites W2267974958 @default.
• W1971597564 cites W2278495047 @default.
• W1971597564 cites W2312098387 @default.
• W1971597564 cites W2318723956 @default.

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