Signal transduction systems of achatin-I,a neuropeptide having a D-phenylalanine residue.

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The effect of intracellular signal transduction system inhibitors on the inward current (I_<in>) caused by achatin-I,an Achatina endogenous tetrapeptide having a D-phenylalanine residue, applied locally onto the neurone tested, were examined under voltage clamp using two identifiable Achatina giant neurone types, v-RCDN and PON.H-89 (PKA inhibitor) markedly suppressed the achatin-I-induced I_<in> on PON, whereas this drug was ineffective on the I_<in> of v-RCDN.Dose (pressure duration)-response study of achatin-I on PON in a physiological solution and in the presence of H-89, and Lineweaver-Burk plot of these data, indicated that H-89 inhibited the I_<in> in noncompetitive manner. KT5823 (PKG inhibitor) suppressed the achatin-I-induced I_<in> of v-RCDN in mainly noncompetitive and partly uncompetitive manners, but this drug had no effect on the I_<in> of PON.W-7 (calmodulin inhibitor) suppressed noncompetitively the I_<in> of PON,but this drug had no effect on the I_<in> of v-RCDN.IBMX (cyclic nucleotide phophodiesterase inhibitor) enhanced the achatin-I-induced I_<in> of v-RCDN,but this drug was ineffective on the I_<in> of PON.However, IBMX might have effects on the achatin-I receptor sites on v-RCDN.These findings suggest multiple intracellular signal transduction pathways mediating the achatin-I-induced I_<in> : the I_<in> of PON is via PKA and probably Ca^<2+>/calmodulin-dependent protein kinase, and the I_<in> of v-RCDN via PKG.Other signal transduction system inhibitors including calphotin C (PKC inhibitor) did not significantly affect the I_<in> of both v-RCDN and PON.