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A nematode FMRFamide-like peptide, SDPNFLRFamide (PF1), relaxes the dorsal muscle strip preparation of Ascaris suum

Published online by Cambridge University Press:  06 April 2009

C. J. Franks ,
L. Holden-Dye ,
R. G. Williams ,
F. Y. Pang  and
R. J. Walker
C. J. Franks
Affiliation:
Department of Physiology and Pharmacology, University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK
L. Holden-Dye
Affiliation:
Department of Physiology and Pharmacology, University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK
R. G. Williams
Affiliation:
Department of Physiology and Pharmacology, University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK
F. Y. Pang
Affiliation:
Department of Physiology and Pharmacology, University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK
R. J. Walker
Affiliation:
Department of Physiology and Pharmacology, University of Southampton, Bassett Crescent East, Southampton SO9 3TU, UK
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Summary

PF1 (SDPNFLRFamide) is a FMRFamide-like peptide extracted from the free-living nematode Panagrellus redivivus. Here we show that this peptide causes a hyperpolarization of somatic muscle cells of the parasitic nematode Ascaris suum and a relaxation of the somatic muscle strip preparation. We have assessed whether or not the relaxation of Ascaris dorsal 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 the Ascaris dorsal 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 hyperpolarizes Ascaris muscle by a mechanism that does not involve stimulation of GABA release from inhibitory pre-synaptic terminals.

Keywords

AscarisnematodeFMRFamidePF1
Type
Research Article
Information
Parasitology , Volume 108 , Issue 2 , February 1994 , pp. 229 - 236
Copyright
Copyright © Cambridge University Press 1994

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