title: Different effects of removing extracellular Ca2+ on cytosolic Ca2+ response to anoxia of sensory neurons and carotid chemoreceptor cells from newborn rabbits.
abstract: To study the mechanism of the increases in cytosolic Ca2+ ([Ca2+]i) induced by anoxia, the author examined the effect of removing extracellular Ca2+ on the [Ca2+]i response in cultured nodose ganglion neurons (control) and carotid body glomus cells prepared from newborn rabbits using a fura-2 microfluorimetry. The sensory neurons showed a small increase in [Ca2+]i during anoxia which was not affected by the removal of extracellular Ca2+ or D600. On the other hand, in the chemoreceptor glomus cells, Ca2+ removal eliminated the anoxia-induced large [Ca2+]i increase in 85% of the tested cells (n = 67), and depressed it in the rest. Interestingly, recovery from exposure to an anoxic Ca(2+)-free solution reversibly produced a large and transient rise in [Ca2+]i. The magnitude of this post-anoxic/Ca(2+)-free [Ca2+]i transient correlated with the intensity of the suppression of the [Ca2+]i response to anoxia in Ca(2+)-free solution. Also the [Ca2+]i transient was mostly inhibited by L-type Ca2+ channel blockers (nifedipine and D600), but was not affected by tetrodotoxin. These results suggest that the anoxia-induced large increase in [Ca2+]i were, in most glomus cells, coming from extracellular sources and, in a few cells, from both extracellular sources and from intracellular pools, whereas the slight increase in [Ca2+]i in sensory neurons was probably produced by releasing Ca2+ from intracellular stores. The post-anoxic/Ca(2+)-free [Ca2+]i transient, seen in the chemoreceptor cells alone, may have resulted from modification of the anoxic [Ca2+]i response by Ca2+ removal and involves mostly L-type Ca2+ channels and a few other Ca2+ entry pathways.
authors.affiliation: Department of Physiology, Akita University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Sato
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002344:Carotid Body / Q000187:drug effects / Q000378:metabolism*; D002478:Cells, Cultured; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000378:metabolism; D003592:Cytophotometry; D003600:Cytosol / Q000378:metabolism*; D017136:Ion Transport / Q000187:drug effects; D009475:Neurons, Afferent / Q000187:drug effects / Q000378:metabolism*; D009620:Nodose Ganglion / Q000187:drug effects / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism*; D011817:Rabbits; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D010100:Oxygen; D002118:Calcium