title: Is the osteoclast calcium "receptor" a receptor-operated calcium channel?
abstract: Elevated extracellular calcium levels ([Ca2+]e) inhibit osteoclast function by elevating cytosolic free calcium levels ([Ca2+]i), presumably via the activation of a surface Ca2+ "receptor". It is unclear whether or not Ca(2+)-induced [Ca2+]i elevation involves the direct gating, by the putative "receptor", of a divalent cation channel. The results show that [Ca2+]i elevation in response to elevated [Ca2+]e comprises a distinct component of Ca2+ influx, the magnitude of which can be decreased and increased, respectively, by depolarising (100 mM-[K+]) and hyperpolarising (1 microM-[valinomycin]) the osteoclast membrane. In addition, activation of the putative Ca2+ "receptor" by elevated [Ca2+]e causes influx of the related divalent cation, magnesium (Mg2+). We suggest that Ca2+ influx induced by Ca2+ "receptor" activation is a major component of the observed [Ca2+]i response.
authors.affiliation: Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, London, U.K.
authors.forename: C M
authors.initials: CM
authors.lastname: Bax
authors.forename: V S
authors.initials: VS
authors.lastname: Shankar
authors.forename: B S
authors.initials: BS
authors.lastname: Moonga
authors.forename: C L
authors.initials: CL
authors.lastname: Huang
authors.forename: M
authors.initials: M
authors.lastname: Zaidi
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D005269:Femur; D008274:Magnesium / Q000378:metabolism; D008564:Membrane Potentials; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D015398:Signal Transduction / Q000187:drug effects; D013977:Tibia; D014634:Valinomycin / Q000494:pharmacology
chemical_list: D015220:Calcium Channels; D014634:Valinomycin; D008274:Magnesium; D011188:Potassium; D002118:Calcium