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Neurobiol."],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We report that cell survival after neurite transection in a mammalian neuronal model (cultured B104 cells) critically depends on somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>, a novel result that reconciles separate long\u2010standing observations that somal survival decreases with more\u2010proximal axonal transections and that increased somal Ca<jats:sup>2+<\/jats:sup> is cytotoxic. Using fluorescence microscopy, we demonstrate that extracellular Ca<jats:sup>2+<\/jats:sup> at the site of plasmalemmal transection is necessary to form a plasmalemmal barrier, and that other divalent ions (Ba<jats:sup>2+<\/jats:sup>, Mg<jats:sup>2+<\/jats:sup>) do not play a major role. We also show that extracellular Ca<jats:sup>2+<\/jats:sup>, rather than injury per se, initiates the formation of a plasmalemmal barrier and that a transient increase in somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> significantly decreases the percentage of cells that survive neurite transection. Furthermore, we show that the increased somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and decreased cell survival following proximal transections are not due to less frequent or slower plasmalemmal sealing or Ca<jats:sup>2+<\/jats:sup> entry through plasmalemmal Na<jats:sup>+<\/jats:sup> and Ca<jats:sup>2+<\/jats:sup> channels. Rather, the increased somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and lethality of proximal neurite injuries may be due to the decreased path length\/increased diameter for Ca<jats:sup>2+<\/jats:sup> entering the transection site to reach the soma. A ryanodine block of Ca<jats:sup>2+<\/jats:sup> release from internal stores before transection has no effect on cell survival; however, a ryanodine\u2010 or thapsigargin\u2010induced buildup of somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> before transection markedly reduces cell survival, suggesting a minor involvement of Ca<jats:sup>2+<\/jats:sup>\u2010induced release from internal stores. Finally, we show that cell survival following proximal injuries can be enhanced by increasing intracellular Ca<jats:sup>2+<\/jats:sup> buffering capacity with BAPTA to prevent the increase in somal [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. \u00a9 2004 Wiley Periodicals, Inc. J Neurobiol 60: 137\u2013153, 2004<\/jats:p>","DOI":"10.1002\/neu.20005","type":"journal-article","created":{"date-parts":[[2004,4,16]],"date-time":"2004-04-16T22:02:19Z","timestamp":1082152939000},"page":"137-153","source":"Crossref","is-referenced-by-count":19,"title":["Survival of mammalian B104 cells following neurite transection at different locations depends on somal Ca<sup>2+<\/sup> concentration"],"prefix":"10.1002","volume":"60","author":[{"given":"Soonmoon","family":"Yoo","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane E.","family":"Bottenstein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George D.","family":"Bittner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harvey 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