Picture of smart phone in human hand

World leading smartphone and mobile technology research at Strathclyde...

The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including by Strathclyde researchers from the Department of Computer & Information Sciences involved in researching exciting new applications for mobile and smartphone technology. But the transformative application of mobile technologies is also the focus of research within disciplines as diverse as Electronic & Electrical Engineering, Marketing, Human Resource Management and Biomedical Enginering, among others.

Explore Strathclyde's Open Access research on smartphone technology now...

Neuromuscular effects of a toxic phospholipase A2 and its nontoxic homologue from the venom of the sea snake, Laticauda colubrina

Rowan, E.G. and Harvey, Alan L. and Takasaki, C. and Tamiya, N. (1989) Neuromuscular effects of a toxic phospholipase A2 and its nontoxic homologue from the venom of the sea snake, Laticauda colubrina. Toxicon, 27 (5). pp. 587-91. ISSN 0041-0101

Full text not available in this repository. Request a copy from the Strathclyde author

Abstract

A single chain phospholipase A2 (LcPLA-II) and a homologous protein lacking enzymatic activity (LcPLH-I) isolated from the venom of the Solomon Island sea snake (Laticauda colubrina) were tested for effects on neuromuscular transmission and muscle contractility on chick biventer cervicis and mouse hemidiaphragm preparations. LcPLA-II (7.5 nM-1.5 microM) blocked indirectly elicited muscle contractions of both preparations. Low concentrations of LcPLA-II caused little change in sensitivity to acetylcholine, carbachol and KCl. The homologue LcPLH-I (375 nM-1.5 microM) reduced the responses of the biventer cervicis preparation to indirect stimulation and abolished responses to acetylcholine and carbachol, but it did not block KCl responses. These effects were due to minor contamination by a post-junctional neurotoxin. LcPLH-I (375 nM-750 nM) had no effect on indirectly stimulated hemidiaphragm preparations. It is concluded that LcPLA-II blocks neuromuscular transmission by a prejunctional action, and that the homologue lacking phospholipase A2 activity also lacks neuromuscular activity.