Major role of dihydropyridine-sensitive Ca2+ channels in Ca (2+) -induced calcitonin secretion
Scherübl, H.; Kleppisch, T.; Zink, A.; Raue, F.; Krautwurst, D.; Hescheler, J.
American Journal of Physiology 264(3 Pt 1): E354-E360
1993
ISSN/ISBN: 0002-9513 PMID: 8384790 Document Number: 414706
Endocrine cells are known to possess multiple types of Ca2+ channels. In neurons, q-conotoxin-sensitive N-type Ca2+ channels have been shown to play a dominant role in neurotransmitter release, but uncertainty remains about the types of Ca2+ channels involved in stimulus-secretion coupling in endocrine cells. We investigated the relative contribution of 1,4-dihydropyridine-sensitive and q-conotoxin-sensitive Ca2+ channels to Ca2+-induced calcitonin release in parafollicular cells of the thyroid (C cells). In whole cell voltage-clamp experiments, both 1,4-dihydropyridine-sensitive and q-conotoxin-sensitive Ca2+ channel currents were identified. The dihydropyridine isradipine (1 mM) but not q-conotoxin (1 mM) inhibited the steady-state Ca2+ influx at physiological membrane potentials, the spontaneous electrical activity, and calcitonin secretion (at 2-h incubations). Moreover, suppression of the spontaneous electrical activity by the Na+ channel blocker tetrodotoxin did not affect calcitonin release. We conclude that 1,4-dihydropyridine-sensitive Ca2+ channels play a major role in Ca2+-dependent calcitonin release and that calcitonin secretion due to Ca2+ influx proceeds even in the absence of action potentials. Reprinted by permission of the publisher.