Ca entry upon depolarization of nerve.
The data reviewed and the experiments presented show that a steady depolarization of a squid giant axon membrane leads to a large but transient Ca entry that is virtually totally dependent upon [Na]i. Since conventional membrane channels do not behave in this way whereas a countertransport reaction is defined as one requiring the participation of ions on opposite sides of the membrane, it is considered reasonable to identify the Ca entry that has been measured as a Na/Ca exchange. Since the enhanced Ca entry is initiated by a reduction in membrane potential, a further conclusion is that the Na/Ca exchange reaction involves a non-electroneutral exchange of changes. The physiological importance of these findings of a Nai-dependent Ca influx in nerve may be that it assures larger Ca entries following rapid tetanic stimulation (because of the increase in Nai) and this may be necessary to produce a Cai signal that is detectable over the increased Cai background as a result of the tetanic stimulation. In smooth and cardiac muscle, increases in Nai surely play a regulatory role in increasing Ca entry with depolarization and hence in increasing tension.
D000818:Animals; D001369:Axons / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000502:physiology; D049832:Decapodiformes; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000502:physiology; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology; D001468:Thoracica
D007473:Ion Channels; D013779:Tetrodotoxin; D012964:Sodium; D011188:Potassium; D002118:Calcium