Conopressin G, a molluscan vasopressin-like peptide, when superfused over the abdominal ganglion suppressed gill withdrawal reflex behavior patterns. The effects of conopressin G on Aplysia californica central sensory neurons and on the sensory neuron to motor neuron synapse were inconsistent with its behavioral effects. That is, superfusion of the peptide facilitated synaptic transmission at this synapse and reversed low-frequency homosynaptic depression. Further, conopressin G potentiated frequency-dependent spike broadening, reduced spike threshold and reduced accommodation. A voltage-dependent outward K+ current was suppressed by the peptide. This current was also suppressed by Co2+ and Ba2+ and was relatively resistant to tetraethylammonium and 4-aminopyridine. The effects produced by conopressin G on the sensory neurons were not observed when Ca2+ was removed from the saline, when a low-Ca2+, high-Mg2+ saline was used or when other procedures that impair synaptic transmission were used. These results suggest that the effects of conopressin G were mediated by a polysynaptic pathway acting on the sensory neurons.

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