title: Mediation of the depolarization-induced [Ca(2+)]i increase in rat sublingual acini by acetylcholine released from nerve terminals.
abstract: In sublingual mucous acini, membrane depolarization induces a threefold transient increase in cytosolic free Ca(2+) concentration [(Ca(2+))i]. The underlying mechanism was examined by using the Ca(2+) sensitive fluorescent indicator fura-2. Membrane depolarization with high K+ induced a transient [Ca(2+)]i increase in acini, but not in single acinar cells. Atropine, pirenzepine and 4-diphenylacetoxy-N-methylpiperidine methiodide prevented the[Ca(2)+]i increase, suggesting the involvement of muscarinic receptor activation. Inhibition of the inositol trisphosphate (IP3)-sensitive Ca(2+) release pathway with S-(diethylamino)-octyl-3,4,5-trimethoxybenzoate prevented the depolarization-induced increase in [Ca(2+)]i. Blockade of nicotinic receptors and L-, N-, and P-type voltage-dependent Ca(2+) channels (hexamethonium, nifedipine, diltiazem, (omega-conotoxin GVIA and omega-agatoxin IVA) did not inhibit the increase in [Ca(2+)]i. However, Cd(2)+ (0.2 mM) blocked >85 percent of the [Ca2+]i increase. The depolarization-induced [Ca(2+)]i increase was also extracellular Ca(2+)-dependent. These results suggest that the membrane depolarization-induced Ca(2+) increase in sublingual acini is mediated by activating Cd(2+)-sensitive, voltage-dependent Ca(2+) channels in nerve terminals associated with the dispersed acini and stimulating release of acetylcholine, which then triggers the [Ca(2+)]i increase in acinar cells.
authors.affiliation: Department of Dental Research, University of Rochester, NY 14642, USA.
authors.forename: G H
authors.initials: GH
authors.lastname: Zhang
authors.forename: B
authors.initials: B
authors.lastname: Chang
authors.forename: J E
authors.initials: JE
authors.lastname: Melvin
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000032:analysis* / Q000037:antagonists & inhibitors / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D003600:Cytosol / Q000737:chemistry; D005456:Fluorescent Dyes; D016257:Fura-2; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D015544:Inositol 1,4,5-Trisphosphate / Q000037:antagonists & inhibitors; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D010890:Pirenzepine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011978:Receptors, Nicotinic / Q000187:drug effects; D013361:Sublingual Gland / Q000187:drug effects / Q000378:metabolism*
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D005456:Fluorescent Dyes; D018727:Muscarinic Antagonists; D018733:Nicotinic Antagonists; D010880:Piperidines; D011978:Receptors, Nicotinic; D002104:Cadmium; D010890:Pirenzepine; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D001285:Atropine; C042375:4-diphenylacetoxy-1,1-dimethylpiperidinium; D015544:Inositol 1,4,5-Trisphosphate; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D016257:Fura-2