Author:
Franks C. J.,Holden-Dye L.,Williams R. G.,Pang F. Y.,Walker R. J.
Abstract
SUMMARYPF1 (SDPNFLRFamide) is a FMRFamide-like peptide extracted from the free-living nematodePanagrellus redivivus. Here we show that this peptide causes a hyperpolarization of somatic muscle cells of the parasitic nematodeAscaris suumand a relaxation of the somatic muscle strip preparation. We have assessed whether or not the relaxation ofAscarisdorsal muscle strip by PF1 is due to (i) inhibition of the release of the excitatory neuromuscular junction transmitter acetylcholine (ACh), (ii) potentiation of the release of the inhibitory neuromuscular junction transmitter γ-aminobutyric acid (GABA) or (iii) a direct inhibitory action of the peptide on the muscle cells. Under the experimental conditions described here, tonic ACh release does not seem to be involved in determining the resting membrane potential or resting tone of theAscarisdorsal muscle strip and thus inhibition of tonic ACh release is unlikely to explain the relaxation elicited by the peptide. Furthermore, PF1 (100 nM–1 μM) inhibited the contraction of the muscle strip elicited by bath application of ACh, suggesting either a direct inhibitory action of the peptide on the muscle cells or a potentiation of GABA release. In electrophysiological experiments, the reversal potential for the PF1 hyperpolarization was not the same as that for GABA. Thus, PF1 hyperpolarizesAscarismuscle by a mechanism that does not involve stimulation of GABA release from inhibitory pre-synaptic terminals.
Publisher
Cambridge University Press (CUP)
Subject
Infectious Diseases,Animal Science and Zoology,Parasitology
Cited by
52 articles.
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