Volume 24, Issue 3 pp. 231-245
Article
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Studies involving avermectin and the 4-aminobutyric acid (GABA) receptor of Ascaris suum muscle

Lindy Holden-Dye

Lindy Holden-Dye

Department of Neurophysiology, School of Biochemical & Physiological Sciences Basset Crescent East, University of Southampton, Southampton SO9 3TU, UK

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Graham M. Hewitt

Graham M. Hewitt

Department of Neurophysiology, School of Biochemical & Physiological Sciences Basset Crescent East, University of Southampton, Southampton SO9 3TU, UK

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Kenneth T. Wann

Kenneth T. Wann

Clinical Research Centre, Watford Road, Harrow, Middlesex HAI 3UJ, UK

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Povl Krogsgaard-Larsen

Povl Krogsgaard-Larsen

Royal Danish School of Pharmacy, Department of Chemistry BC, Universitets Parken 2, DK-2100 Copenhagen, Denmark

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Robert J. Walker

Robert J. Walker

Department of Neurophysiology, School of Biochemical & Physiological Sciences Basset Crescent East, University of Southampton, Southampton SO9 3TU, UK

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First published: 1988
Citations: 48

Based on a poster presented at Neurotox 88—an International Symposium on Neuropharmacology and Pesticide Action, organised by the Society of Chemical industry on 11-15 April. 1988, at the University of Nottingham.

Abstract

This study describes the pharmacology of the Ascaris suum muscle GABA receptor using a range of GABA agonists and antagonists. The GABA receptor at this site does not readily fit into GABA-A or GABA-B classification. The effect of the potent anthehmintic, avermectin, on these cells was investigated. It was found to inhibit GABA-evoked increase in membrane conductance and membrane hyper polarisation on quiescent muscle cells with an apparent affinity constant in the mid-micromolar range. When applied to spontaneously active muscle cells, avermectin (I üM) inhibited the spiking activity after a delay of about 25 min.

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