Mediation of the depolarization-induced [ca 2+] i increase in rat sublingual acini by acetylcholine released from nerve terminals

• Published in: Archives of oral biology 1996, Vol.41 (1), p.85-90
• Main Authors: H. Zhang, Guo, Chang, Benjamin, E. Melvin, James
• Format: Article
• Language: English
• Subjects: Acetylcholine - metabolism; Animals; Atropine - pharmacology; Ca 2; Cadmium - pharmacology; Calcium - analysis; Calcium - antagonists & inhibitors; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Calcium Channels - drug effects; Calcium Channels - metabolism; Cell Membrane - drug effects; Cell Membrane - metabolism; Cytosol - chemistry; Dentistry; depolarization; Fluorescent Dyes; Fura-2; Gallic Acid - analogs & derivatives; Gallic Acid - pharmacology; Inositol 1,4,5-Trisphosphate - antagonists & inhibitors; Male; Muscarinic Antagonists - pharmacology; Nerve Endings - drug effects; Nerve Endings - metabolism; nerve terminals; Nicotinic Antagonists - pharmacology; Piperidines - pharmacology; Pirenzepine - pharmacology; Potassium - pharmacology; Rats; Rats, Wistar; Receptors, Nicotinic - drug effects; sublingual acini; Sublingual Gland - drug effects; Sublingual Gland - metabolism
• ISSN: 0003-9969; 1879-1506
• DOI: 10.1016/0003-9969(95)00087-9

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 Call-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 OP,)-sensitive Ca 2+ release pathway with 8-(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, ω-conotoxin GVIA and ω-agatoxin IVA) did not inhibit the increase in [Ca 2+] i. However, Cd 2+ (0.2 mM) blocked > 85% of the [Ca 2+] i increase. The depolarizationinduced [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.