{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T12:09:18Z","timestamp":1790856558867,"version":"4.1.0"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1979,1,1]],"date-time":"1979-01-01T00:00:00Z","timestamp":283996800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1979,1]]},"abstract":"<jats:p>1. 22Na+ and 45Ca2+ fluxes were studied in the clonal nerve cell line PC12. Three distinct types of ion channels were found: (a) voltage\u2010dependent  Na+ channels, (b) voltage\u2010dependent Ca2+ channels, and (c) acetylcholine\u2010activated channels permeable to both ions. 2. 22Na+ uptake through voltage\u2010dependent Na+ channels is induced by veratridine and scorpion venom, and is inhibited 50% by 5 X 10(\u20107) M\u2010tetrodotoxin and greater than 98% by 5 X 10(\u20106) M\u2010tetrodotoxin. 3. 45Ca2+ uptake through voltage\u2010dependent Ca2+ channels is induced by depolarizing the cells in 50 mM\u2010KCl. This flux is not dependent on the presence of Na+ in the medium and is insensitive to 5 X 10(\u20106) M\u2010tetrodotoxin. However, 1 mM\u2010Mn2+ causes a 95% inhibition of K+\u2010induced 45Ca2+ uptake. 4. Veratridine and scorpion venom also induce voltage\u2010dependent 45Ca2+ uptake which can be blocked by 1mM\u2010Mn2+. In contrast to KCl\u2010induced 45Ca2+ uptake, this flux is completely blocked by 5 X 10(\u20106) M\u2010tetrodotoxin and is abolished by removal of Na+ from the medium. Thus the depolarizing stimulus for Ca2+ uptake in this case is Na+ from the medium. Thus the depolarizing stimulus for Ca2+ uptake in this case is Na+ influx through voltage\u2010dependent Na+ channels. 5. Carbamylcholine induces both 22Na+ and 45Ca2+ fluxes which are blocked by nicotinic cholinergic antagonists with the exception of alpha\u2010bungarotoxin. The 22Na+ flux occurs exclusively via acetylcholine receptor channels, as evidenced by the lack of effect of 5 X 10(\u20106) M\u2010tetrodotoxin. In the presence of Na+, almost all of the 45Ca2+ uptake can be blocked by 1 mM\u2010Mn2+ and thus occurs via voltage\u2010dependent Ca2+ channels which are activated by the depolarizing Na+ influx. 6\u2010\u20108% of the total 45Ca2+ flux, however, is insensitive to 1 mM\u2010Mn2+, suggesting that this portion of the uptake occurs via the acetylcholine receptor channels. In Na+\u2010free medium, the Mn2+\u2010resistant 45Ca2+ component increases to 40% of the total uptake, apparently due to lack of competition from Na+ for the acetylcholine receptor channels. This receptor\u2010linked flux still causes sufficient depolarization to induce the additional 60% of the Ca2+ flux through voltage\u2010dependent, Mn2+ sensitive Ca2+ channels. 6. Mn2+ inhibits Ca2+ flux through voltage\u2010dependent Ca2+ channels by competing for entry through these channels. 50 mM\u2010KCl induces 54Mn2+ fluxes in PC12 cells that are comparable in magnitude to 45Ca2+ fluxes. 7. In normal saline 45Ca2+ efflux from PC12 cells is several times more rapid than in Na+\u2010free medium, indicating the presence of a Ca2+\u2010Na+ exchange mechanism.<\/jats:p>","DOI":"10.1113\/jphysiol.1979.sp012635","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T07:32:45Z","timestamp":1418974365000},"page":"525-540","source":"Crossref","is-referenced-by-count":116,"title":["Sodium and calcium fluxes in a clonal nerve cell line."],"prefix":"10.1113","volume":"286","author":[{"given":"W B","family":"Stallcup","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1979,1]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1979.sp012635","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1979.sp012635","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,5]],"date-time":"2023-11-05T18:25:45Z","timestamp":1699208745000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1979.sp012635"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1979,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1979,1]]}},"alternative-id":["10.1113\/jphysiol.1979.sp012635"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1979.sp012635","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1979,1]]}}}