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Studies on the actions of the nematode FMRFamide-like neuropeptide PF1

Studies on the actions of the nematode FMRFamide-like neuropeptide PF1
Studies on the actions of the nematode FMRFamide-like neuropeptide PF1

Electrophysiological and organ bath techniques were employed to elucidate the actions of PF1 (SDPNFLRFamide), in the neuromuscular system of Ascaris suum. An Ascaridia galli organ bath assay was used to compare the action of PF1 and related structural analogues. Immunohistochemistry was used to estimate the distribution of RFamide-like peptides in the nervous system of A.suum.

FMRFamide-like and KYSALMFamide-like immunoreactivity was widespread in the nervous system of A.suum. In particular, immunoreactivity was localised within inhibitory and excitatory motoneurons, indicating that FMRFamide-like neuropeptides may subserve an important role within the neuromuscular system of the worm.

PF1, extracted from Panagrellus redivivas, elicits a potent inhibitory effect of A.suum muscle. In organ bath experiments, PF1 reduced the resting tension of somatic muscle and contractions elicited by ACh. In an electrophysiological study, PF1 caused a dose-dependent hyperpolarisation of muscle cells (EC50=349 ± 87 nM) and inhibited spontaneous electrical activity. However it failed to elicit any consistent change in input conductance. PF1 also failed to elicit an effect on conductance changes and the amplitude of depolarisations, elicited by bath applied ACh.

In a low chloride medium (40.1 mM), the reversal potential for GABA was -28 ± 0.8 mV, close to the theoretical equilibrium potential for chloride ions, whereas the PF1 reversal potential was outside the range of current-voltage plots. This indicated that the GABA response is chloride mediated, but that the PF1 response is not. Furthermore, the GABA antagonist SN 612239 (10 μM), reversibly blocked GABA hyperpolarisations but failed to block hyperpolarisations elicited by PF1. Therefore, PF1 does not elicit an inhibition of muscle cells by increasing presynaptic release of GABA.

University of Southampton
Franks, Christopher John
Franks, Christopher John

Franks, Christopher John (1996) Studies on the actions of the nematode FMRFamide-like neuropeptide PF1. University of Southampton, Doctoral Thesis.

Record type: Thesis (Doctoral)

Abstract

Electrophysiological and organ bath techniques were employed to elucidate the actions of PF1 (SDPNFLRFamide), in the neuromuscular system of Ascaris suum. An Ascaridia galli organ bath assay was used to compare the action of PF1 and related structural analogues. Immunohistochemistry was used to estimate the distribution of RFamide-like peptides in the nervous system of A.suum.

FMRFamide-like and KYSALMFamide-like immunoreactivity was widespread in the nervous system of A.suum. In particular, immunoreactivity was localised within inhibitory and excitatory motoneurons, indicating that FMRFamide-like neuropeptides may subserve an important role within the neuromuscular system of the worm.

PF1, extracted from Panagrellus redivivas, elicits a potent inhibitory effect of A.suum muscle. In organ bath experiments, PF1 reduced the resting tension of somatic muscle and contractions elicited by ACh. In an electrophysiological study, PF1 caused a dose-dependent hyperpolarisation of muscle cells (EC50=349 ± 87 nM) and inhibited spontaneous electrical activity. However it failed to elicit any consistent change in input conductance. PF1 also failed to elicit an effect on conductance changes and the amplitude of depolarisations, elicited by bath applied ACh.

In a low chloride medium (40.1 mM), the reversal potential for GABA was -28 ± 0.8 mV, close to the theoretical equilibrium potential for chloride ions, whereas the PF1 reversal potential was outside the range of current-voltage plots. This indicated that the GABA response is chloride mediated, but that the PF1 response is not. Furthermore, the GABA antagonist SN 612239 (10 μM), reversibly blocked GABA hyperpolarisations but failed to block hyperpolarisations elicited by PF1. Therefore, PF1 does not elicit an inhibition of muscle cells by increasing presynaptic release of GABA.

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Published date: 1996

Identifiers

Local EPrints ID: 459813
URI: http://eprints.soton.ac.uk/id/eprint/459813
PURE UUID: 83b1c122-bce1-486f-8cc4-cc3f6c336e92

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Date deposited: 04 Jul 2022 17:19
Last modified: 04 Jul 2022 17:19

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Author: Christopher John Franks

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