{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T09:15:27Z","timestamp":1762161327363},"reference-count":57,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2000,1,1]]},"abstract":"<jats:p>Intracellular Ca<jats:sup>2+<\/jats:sup>([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) was fluorometrically measured with fura-2 in lumbar motoneurons of acutely isolated spinal cord slices from embryonic rats. In ester-loaded cells, bath-applied glutamate (3 \u03bcM to 1 mM) evoked a [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase by up to 250 nM that was abolished by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) plus 2-amino-5-phosphonovalerate (APV). CNQX or APV alone reduced the response by 82 and 25%, respectively. The glutamatergic agonists kainate (KA), quisqualate (QUI), and S-\u03b1-amino-3-hydroxy-5-methyl-4-isoxalone (S-AMPA) evoked a similar [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>transient as glutamate. N-methyl-d-aspartate (NMDA) was only effective to increase [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>in Mg<jats:sup>2+<\/jats:sup>-free saline, whereas [1S,3R]-1-aminocyclopentane-1,3-dicarboxylic acid ([1S,3R]-ACPD) had no effect. The glutamate-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>rise was suppressed in Ca<jats:sup>2+<\/jats:sup>-free superfusate. Depletion of Ca<jats:sup>2+<\/jats:sup>stores with cyclopiazonic acid (CPA) did not affect the response. Thirty-six percent of the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase in response to membrane depolarization induced by a 50 mM K<jats:sup>+<\/jats:sup>solution persisted on combined application of the voltage-gated Ca<jats:sup>2+<\/jats:sup>channel blockers nifedipine, \u03c9-conotoxin-GVIA and \u03c9-agatoxin-IVA. In fura-2 dialyzed motoneurons, the glutamate-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>increase was attenuated by \u223c70% after changing from current to voltage clamp. Forty percent of the remaining [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>transient and 20% of the concomitant inward current of 0.3 nA were blocked by Joro spider toxin-3 (JSTX). The results show that voltage-gated Ca<jats:sup>2+<\/jats:sup>channels, including a major portion of R-type channels, constitute the predominant component of glutamate-induced [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>rises. NMDA and Ca<jats:sup>2+<\/jats:sup>-permeable KA\/AMPA receptors contribute about equally to the remaining component of the Ca<jats:sup>2+<\/jats:sup>rise. The results substantiate previous assumptions that Ca<jats:sup>2+<\/jats:sup>influx through JSTX-sensitive KA\/AMPA receptors is involved in (trophic) signaling in developing motoneurons.<\/jats:p>","DOI":"10.1152\/jn.2000.83.1.50","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T12:32:49Z","timestamp":1513859569000},"page":"50-59","source":"Crossref","is-referenced-by-count":22,"title":["Contribution of Ca<sup>2+<\/sup>-Permeable AMPA\/KA Receptors to Glutamate-Induced Ca<sup>2+<\/sup>Rise in Embryonic Lumbar Motoneurons In Situ"],"prefix":"10.1152","volume":"83","author":[{"given":"Friedrich","family":"Metzger","sequence":"first","affiliation":[{"name":"Klinische Forschergruppe Neuroregeneration, Neurologische Klinik, Universit\u00e4t W\u00fcrzburg, D-97080 Wurzburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anna","family":"Kulik","sequence":"additional","affiliation":[{"name":"II. 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