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Voltage‐activated calcium currents in presynaptic nerve terminals of the chicken ciliary ganglion.
Author(s) -
Yawo H
Publication year - 1990
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1990.sp018207
Subject(s) - depolarization , nifedipine , chemistry , biophysics , ciliary ganglion , calcium , voltage dependent calcium channel , electrophysiology , neuroscience , biology , organic chemistry
1. Calcium currents (ICa) were recorded from presynaptic calyces of ciliary ganglia of the chick embryo under whole‐cell voltage clamp. 2. Only high‐threshold ICa was recorded without any evidence for the presence of low‐threshold Ca2+ channels. 3. High‐threshold (high‐voltage‐activated, HVA) ICa could be classified into non‐inactivating (HVAn) and inactivating (HVAi) components. The mean inactivation time constant of the HVAi component was 213 ms (at 0 mV). The threshold for activation by depolarizing pulses was more negative for the HVAn component than for the HVAi component. The HVAi component was inactivated by 19% at a holding potential of ‐60 mV, while the HVAn component was little affected under this condition. 4. The activation of HVAn component was faster than that of the HVAi component. 5. Both the HVAn and HVAi components were blocked by Cd2+ (50 microM) and La3+ (1 microM). Both components were only slightly affected by Ni2+ (100 microM). The order of potency in blocking was La3+ greater than Cd2+ greater than Ni2+ for both components. Both the HVAi and HVAn components were irreversibly blocked by omega‐conotoxin GVIA(omega‐CgTX, 10 microM). 6. The two components could pharmacologically be distinguished by selective blockade of the HVAn component with nifedipine (2 microM) and D600 (100‐250 microM). 7. HVAn and HVAi components are suggested to represent two different subpopulations of Ca2+ channels. The HVAn subpopulation may be responsible for persistent Ca2+ influx during subthreshold depolarization of the nerve terminal.