{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T21:40:13Z","timestamp":1717623613145},"reference-count":29,"publisher":"Cambridge University Press (CUP)","issue":"6","license":[{"start":{"date-parts":[[2014,12,2]],"date-time":"2014-12-02T00:00:00Z","timestamp":1417478400000},"content-version":"unspecified","delay-in-days":1127,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Neurol. Sci."],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:sec id=\"S0317167100012476_abs1\"><jats:title>Background:<\/jats:title><jats:p>Cytosol Ca<jats:sup>2+<\/jats:sup>overload plays a vital role in ischemic neuronal damage, which is largely contributed by the Ca<jats:sup>2+<\/jats:sup>influx through L-type voltage-gated calcium channels (L-VGCCs) and N-methyl-D-aspartate (NMDA) type glutamate receptors. In this article, L-VGCCs were activated by depolarization to investigate the cross-talk between NMDA receptors and L-VGCCs.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012476_abs2\"><jats:title>Methods:<\/jats:title><jats:p>Depolarization was induced by 20 minutes incubation of 75 mM KCl in cultured rat cortical neuron. Apoptosis-like neuronal death was detected by DAPI staining. Tyrosine phosphorylation of NMDA receptor subunit 2A (NR2A), interactions of Src and NR2A were detected by immunoblot and immunoprecipitation.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012476_abs3\"><jats:title>Results:<\/jats:title><jats:p>Depolarization induced cortical neuron apoptosis-like cell death after 24 hours of restoration. The apoptosis was partially inhibited by 5 mM EGTA, 100 \u03bcM Cd<jats:sup>2+<\/jats:sup>, 10 \u03bcM nimodipine, 100 \u03bcM genistein, 20 \u03bcM MK-801, 2 \u03bcM PP2 and combined treatment of nimodipine and MK-801. NR2A tyrosine phosphorylation increased after depolarization, and the increase was inhibited by the drugs listed above. Moreover, non-receptor tyrosine kinase Src bound with NR2A after depolarization and restoration. The binding was also inhibited by the drugs listed above.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012476_abs4\"><jats:title>Conclusions:<\/jats:title><jats:p>The results indicated that depolarization-induced neuronal death might be due to extracellular Ca<jats:sup>2+<\/jats:sup>influx through L-VGCCs and subsequently Src activationmediated NR2A tyrosine phosphorylation.<\/jats:p><\/jats:sec>","DOI":"10.1017\/s0317167100012476","type":"journal-article","created":{"date-parts":[[2014,12,12]],"date-time":"2014-12-12T15:09:56Z","timestamp":1418396996000},"page":"880-886","source":"Crossref","is-referenced-by-count":1,"title":["Depolarization Induces NR2A Tyrosine Phosphorylation and Neuronal 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