{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T22:42:24Z","timestamp":1790548944272,"version":"4.1.0"},"reference-count":0,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1997,3,1]],"date-time":"1997-03-01T00:00:00Z","timestamp":857174400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1997,3,15]]},"abstract":"<jats:p>1. We studied regulation of intracellular Na+ concentration ([Na+]i) in cultured rat hippocampal neurones using fluorescence ratio imaging of the Na+ indicator dye SBFI (sodium\u2010binding benzofuran isophthalate). 2. In standard CO2\/HCO3(\u2010)\u2010buffered saline with 3 mM K+, neurones had a baseline [Na+]i of 8.9 +\/\u2010 3.8 mM (mean +\/\u2010 S.D.). Spontaneous, transient [Na+]i increases of 5 mM were observed in neurones on 27% of the coverslips studied. These [Na+]i increases were often synchronized among nearby neurones and were blocked reversibly by 1 microM tetrodotoxin (TTX) or by saline containing 10 mM Mg2+, suggesting that they were caused by periodic bursting activity of synaptically coupled cells. Opening of voltage\u2010gated Na+ channels by application of 50 microM veratridine caused a TTX\u2010sensitive [Na+]i increase of 25 mM. 3. Removing extracellular Na+ caused an exponential decline in [Na+]i to values close to zero within 10 min. Inhibition of Na+,K(+)\u2010ATPase by removal of extracellular K+ or ouabain application evoked a [Na+]i increase of 5 mM min\u20101. Baseline [Na+]i was similar in the presence or absence of CO2\/HCO3\u2010; switching from CO2\/HCO3(\u2010)\u2010free to CO2\/HCO3(\u2010)\u2010buffered saline, however, increased [Na+]i transiently by 3 mM, indicating activation of Na(+)\u2010dependent Cl(\u2010)\u2010HCO3\u2010 exchange. Inhibition of Na(+)\u2010K(+)\u20102Cl\u2010 cotransport by bumetanide had no effect on [Na+]i. 4. Brief, small changes in extracellular K+ concentration ([K+]o) influenced neuronal [Na+]i only weakly. Virtually no change in [Na+]i was observed with elevation or reduction of [K+]o by 1 mM. Only 30% of cells reacted to 3 min [K+]o elevations of up to 5 mM. In contrast, long [K+]o alterations (&gt; or = 10 min) to 6 mM or greater slowly changed steady\u2010state [Na+]i in the majority of cells. 5. Our results indicate several differences between [Na+]i regulation in cultured hippocampal neurones and astrocytes. Baseline [Na+]i is lower in neurones compared with astrocytes and is mainly determined by Na+,K(+)\u2010ATPase, whereas Na(+)\u2010dependent Cl(\u2010)\u2010HCO3\u2010 exchange, Na(+)\u2010HCO3\u2010 cotransport or Na(+)\u2010K(+)\u20102Cl\u2010 cotransport do not play a significant role. In contrast to glial cells, [Na+]i of neurones changes only weakly with small alterations in bath [K+]o, suggesting that activity\u2010induced [K+]o changes in the brain might not significantly influence neuronal Na+,K(+)\u2010ATPase activity.<\/jats:p>","DOI":"10.1113\/jphysiol.1997.sp021951","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T06:18:40Z","timestamp":1418797120000},"page":"573-587","source":"Crossref","is-referenced-by-count":117,"title":["Regulation of intracellular sodium in cultured rat hippocampal neurones."],"prefix":"10.1113","volume":"499","author":[{"given":"C R","family":"Rose","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B R","family":"Ransom","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1997,3]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1997.sp021951","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1997.sp021951","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,27]],"date-time":"2023-10-27T10:39:43Z","timestamp":1698403183000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1997.sp021951"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1997,3]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1997,3,15]]}},"alternative-id":["10.1113\/jphysiol.1997.sp021951"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1997.sp021951","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1997,3]]}}}