Two components of high-threshold Ca2+ current inactivate by different mechanisms.
High-threshold Ca2+ current triggers neurotransmitter release, but the existence, significance, and correct identification of different types of high-threshold Ca2+ channels remain controversial. We show selective inhibition of a rapidly inactivating component of high-threshold Ca2+ current in rat sensory neurons by bursts of brief pulses that mimic trains of action potentials and by prolonged depolarization just above the normal rest potential. In contrast, a slowly inactivating component decreases only when sufficient Ca2+ accumulates within the cell. Thus, there are physiologically important differences: whereas availability of the transient component depends on the value of the rest potential and the pattern of a prior stimulus, the sustained component seems to provide a baseline level of voltage-dependent Ca2+ entry that is lost only when intracellular Ca2+ rises.
Department of Cell Biology and Physiology, Washington University, St. Louis, Missouri 63110.
J E
JE
Schroeder
P S
PS
Fischbach
M
M
Mamo
E W
EW
McCleskey
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004056:Differential Threshold; D004594:Electrophysiology; D008433:Mathematics; D009475:Neurons, Afferent / Q000502:physiology*; D010456:Peptides, Cyclic / Q000494:pharmacology; D013997:Time Factors; D020960:omega-Conotoxins
D002121:Calcium Channel Blockers; D010456:Peptides, Cyclic; D020960:omega-Conotoxins; C053423:Conus magus toxin; D002118:Calcium