Ca2+ currents (ICa) were recorded from the
neurosecretory terminals of the crab X-organ-sinus gland under
voltage-clamp conditions. ICa was detectable at
command potentials above -40 mV, with maximum currents at approximately
+20 mV. No differences were observed between current-voltage
(I/V) relationships from holding potentials of -50 or -90
mV, indicating that there were no low-voltage-activated Ca2+
channels present in the terminals. The decay of ICa
was best fitted with a single exponential, the extent of inactivation
over 50 ms averaging 53 %. The rate of decay of ICa
was reduced by the substitution of Ca2+ with Sr2+
in the external solution and was eliminated by substitution with
Ba2+.
The effect of varying prepulse potential on the amplitude of ICa at +20 mV was tested. ICa declined with increasing prepulse depolarization up to +20 mV and then showed partial recovery at more depolarized prepulse potentials. Inactivation curves in solutions containing Sr2+ and Ba2+ showed much less current-dependent inactivation. Removing Ca2+ chelators from the internal solution significantly increased ICa decay. ICa was insensitive to nifedipine at a concentration of 1 µmol I-1. Pretreatment of the isolated sinus gland containing the intact terminals with a combination of ω-conotoxin (ω-Ctx) GVIA, ω-Ctx MVIIC and ω-agatoxin IVA had no effect on the levels of K+-induced peptide release.
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