FMRFamide neuropeptides simultaneously increase and decrease K+ current in an identified neurone.

Abstract

Phe-Met-Arg-Phe-NH2, or FMRFamide, discovered in ganglia of the clam Macrocallista nimbosa1 has potent cardio-stimulatory activity in some molluscan species, but is cardio-inhibitory in others, and produces contractions of certain non-cardiac muscles2. A peptide with similar properties is present in the ganglia of the snail Helix3, and is thought to differ from the Macrocallista peptide in having one or more additional amino acids combined with the terminal free amino nitrogen. An homologous opiate peptide, Tyr-Gly-GIy-Phe-Met-Arg-Phe (or YGGFMRF, using single letter abbreviations4), was identified in adrenal medullary granules and the striatum5. YGGFMRFamide has chromatographic properties more similar, though not identical, to the Helix peptide than FMRFamide itself (D. A. Price, M. J. Greenberg and G.A.C., unpublished). FMRFamide has potent and complex effects on Helix neurones. One neurone in each cerebral ganglion, the C1 or giant serotonin neurone (GSN), is hyperpolarized by FMRFamide at the resting membrane level, but depolarized at less negative potentials6.I show here that YGGFMRFamide has similar effects to FMRFamide and examine further the ionic mechanisms underlying the two responses of the GSN. The results indicate that the hyperpolarizing, outward current response results from an increase in conductance to K+ whereas the depolarizing response, which was recorded as a reduction in net outward current, is due to the suppression of a Ca2+ activated K+current.