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 -40mV, with maximum currents at approximately +20mV. No differences were observed between current-voltage (I/V) relationships from holding potentials of -50 or -90mV, 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 +20mV was tested. ICa declined with increasing prepulse depolarization up to +20mV 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 mumol l-1. Pretreatment of the isolated sinus gland containing the intact terminals with a combination of omega-conotoxin (omega-Ctx) GVIA, omega-Ctx MVIIC and omega-agatoxin IVA had no effect on the levels of K+-induced peptide release.

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