{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T16:07:42Z","timestamp":1761581262639},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1987,3,1]],"date-time":"1987-03-01T00:00:00Z","timestamp":541555200000},"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":[[1987,3]]},"abstract":"<jats:p>1. Salivary acini were isolated enzymatically from submandibular glands of adult male mice. The patch\u2010clamp technique was employed to record K+ currents in cell\u2010attached patches of basolateral membrane. Application of acetylcholine (10(\u20105) M) to the medium bathing the cells results in a pronounced and sustained activation of the K+ channels in the cell\u2010attached patches, an effect mediated by an intracellular second messenger. In the present study we investigate the mechanism by which acetylcholine achieves activation of K+ channels. 2. The effects of acetylcholine on single\u2010channel activity were shown to be dependent on extracellular Ca2+, i.e. due to Ca2+ influx. In cells bathed in Ca2+\u2010free medium acetylcholine activation resulted in no increase in single\u2010channel open probability. This blockade could be reversed by reintroduction of Ca2+ to the extracellular fluid in the continued presence of the agonist. The effects of acetylcholine in control medium (1.2 mM\u2010Ca2+) were mimicked by the Ca2+ ionophore, A23187 (10(\u20108) M). 3. In K+\u2010depolarized cells (bathed in a Na+\u2010free, 145 mM\u2010KCl solution) there was no evidence of any voltage\u2010activated Ca2+ influx pathway. In the K+\u2010depolarized cells acetylcholine application was no longer associated with any increase in the open probability of the K+ channels. K+ channels could be activated by adding A23187 (10(\u20108) M) to the high\u2010K+ solution. 4. Cells bathed in another Na+\u2010free (N\u2010methyl\u2010D\u2010glucamine substituted for Na+) but non\u2010depolarizing solution were also refractory to acetylcholine. K+ currents could, however, be activated in patches attached to these cells by application of A23187 (10(\u20108) M) or by the introduction of 20 mM\u2010Na+ to the extracellular fluid in the presence of acetylcholine. The increased activity associated with the reintroduction of Na+ was totally reversed by atropine, i.e. it was receptor regulated. 5. The data presented above indicate that the cholinergic regulation of K+ channels is secondary to the receptor\u2010regulated activation of a Ca2+ influx pathway. There is no evidence of voltage\u2010activated Ca2+ influx in these cells. The cholinergic activation of Ca2+ influx is abolished in Na+\u2010depleted cells. We conclude that the Na+ dependency indicates either that Na+ is involved in the gating of some voltage\u2010independent Ca2+ channel or that Ca2+ entry is via a coupled Na+\u2010Ca2+ co\u2010 or countertransport pathway.<\/jats:p>","DOI":"10.1113\/jphysiol.1987.sp016446","type":"journal-article","created":{"date-parts":[[2014,12,19]],"date-time":"2014-12-19T06:42:16Z","timestamp":1418971336000},"page":"119-130","source":"Crossref","is-referenced-by-count":27,"title":["The receptor\u2010regulated calcium influx in mouse submandibular acinar cells is sodium dependent: a patch\u2010clamp study."],"prefix":"10.1113","volume":"384","author":[{"given":"D V","family":"Gallacher","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A P","family":"Morris","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1987,3]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1987.sp016446","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1987.sp016446","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,20]],"date-time":"2023-10-20T14:23:15Z","timestamp":1697811795000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1987.sp016446"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1987,3]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1987,3]]}},"alternative-id":["10.1113\/jphysiol.1987.sp016446"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1987.sp016446","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1987,3]]}}}