{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T16:27:29Z","timestamp":1764174449019},"reference-count":32,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2002,8,1]]},"abstract":"<jats:p>Simultaneous recordings of intracellular Ca<jats:sup>2+<\/jats:sup>([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) signal and extracellular DC potential were obtained from the CA1 region in 1-[6-amino-2-(5-carboxy-2-oxazolyl)-5-benzofuranyloxy]-2-(2-amino-5-methylphenoxy)-ethane- N, N, N\u2032, N\u2032-tetraacetic acid penta-acetoxymethyl ester (Fura-2\/AM)-loaded rat hippocampal slices. Superfusion with oxygen- and glucose-deprived medium (in vitro ischemia) for 5\u20136 min produced a rapid rise of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>level in the stratum radiatum (rising phase of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal), which occurred simultaneously with a rapid negative DC potential (rapid negative potential). When oxygen and glucose were reintroduced, the increased [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal diminished rapidly (falling phase of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal) during the generation of a slow negative DC potential (slow negative potential), which occurred within 1 min from the onset of the reintroduction. Thereafter, the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal partially and the slow negative potential completely returned to the preexposure level approximately 6 min after the reintroduction. The changes in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal during and after in vitro ischemia were very similar to the changes in the membrane potential of glial cells. The rising and falling phases of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal corresponded to the rapid depolarization and a depolarizing hump, respectively, in the repolarizing phase of glial cells. A prolonged application of in vitro ischemia or a reintroduction of either glucose or oxygen suppressed the falling phase after ischemic exposure. The application of ouabain (30 \u03bcM) generated both a rapid negative potential and a rapid elevation of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, but no slow negative potential or rapid reduction in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>were observed. When oxygen and glucose were reintroduced to slices in the Na<jats:sup>+<\/jats:sup>-free or ouabain- or Ni<jats:sup>2+<\/jats:sup>-containing medium, the falling phase was suppressed. The falling phase was significantly accelerated in Ca<jats:sup>2+<\/jats:sup>- and Mg<jats:sup>2+<\/jats:sup>-free with EGTA-containing medium. In contrast, the falling phase was significantly slower in the Ca<jats:sup>2+<\/jats:sup>-free with high Mg<jats:sup>2+<\/jats:sup>- and EGTA-containing medium. The falling phase of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>signal after ischemic exposure is thus considered to be primarily dependent on the reactivation of Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>-ATPases, while the extrusion of cytosolic Ca<jats:sup>2+<\/jats:sup>via the forward-mode operation of Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup>exchangers in glial cells is thought to be directly involved in the rapid reduction of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>after ischemic exposure.<\/jats:p>","DOI":"10.1152\/jn.2002.88.2.879","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T19:55:37Z","timestamp":1513886137000},"page":"879-887","source":"Crossref","is-referenced-by-count":21,"title":["Extrusion of Intracellular Calcium Ion After In Vitro Ischemia in the Rat Hippocampal CA1 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