{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,9,9]],"date-time":"2023-09-09T19:13:26Z","timestamp":1694286806433},"reference-count":50,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2010,9]]},"abstract":"<jats:p>In many brain regions, synchronous neural activity causes a rapid rise in extracellular pH. In the CA1 region of hippocampus, this population alkaline transient (PAT) enhances responses from postsynaptic, pH-sensitive N-methyl-d-aspartate (NMDA) receptors. Recently, we showed that the plasma membrane Ca<jats:sup>2+<\/jats:sup>-ATPase (PMCA), a ubiquitous transporter that exchanges internal Ca<jats:sup>2+<\/jats:sup>for external H<jats:sup>+<\/jats:sup>, is largely responsible for the PAT. It has also been shown that a PAT can be generated after replacing extracellular Ca<jats:sup>2+<\/jats:sup>with Ba<jats:sup>2+<\/jats:sup>. The cause of this PAT is unknown, however, because the ability of the mammalian PMCA to transport Ba<jats:sup>2+<\/jats:sup>is unclear. If the PMCA did not carry Ba<jats:sup>2+<\/jats:sup>, a different alkalinizing source would have to be postulated. Here, we address this issue in mouse hippocampal slices, using concentric (high-speed, low-noise) pH microelectrodes. In Ba<jats:sup>2+<\/jats:sup>-containing, Ca<jats:sup>2+<\/jats:sup>-free artificial cerebrospinal fluid, a single antidromic shock to the alveus elicited a large (0.1\u20130.2 unit pH), \u201call-or-none\u201d PAT in the CA1 cell body region. In whole cell current clamp of single CA1 pyramidal neurons, the same stimulus evoked a prolonged plateau potential that was similarly all-or-none. Using this plateau as the voltage command in other cells, we recorded Ba<jats:sup>2+<\/jats:sup>-dependent surface alkaline transients (SATs). The SATs were suppressed by adding 5 mM extracellular HEPES and abolished when carboxyeosin (a PMCA inhibitor) was in the patch pipette solution. These results suggest that the PAT evoked in the presence of Ba<jats:sup>2+<\/jats:sup>is caused by the PMCA and that this transporter is responsible for the PAT whether Ca<jats:sup>2+<\/jats:sup>or Ba<jats:sup>2+<\/jats:sup>is the charge carrying divalent cation.<\/jats:p>","DOI":"10.1152\/jn.00504.2010","type":"journal-article","created":{"date-parts":[[2010,7,15]],"date-time":"2010-07-15T02:52:07Z","timestamp":1279162327000},"page":"1438-1444","source":"Crossref","is-referenced-by-count":4,"title":["Barium Plateau Potentials of CA1 Pyramidal Neurons Elicit All-or-None Extracellular Alkaline Shifts Via the Plasma Membrane Calcium ATPase"],"prefix":"10.1152","volume":"104","author":[{"given":"Sachin","family":"Makani","sequence":"first","affiliation":[{"name":"Departments of 1Physiology and Neuroscience and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mitchell","family":"Chesler","sequence":"additional","affiliation":[{"name":"Departments of 1Physiology and 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