Picture of a black hole

Strathclyde Open Access research that creates ripples...

The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of research papers by University of Strathclyde researchers, including by Strathclyde physicists involved in observing gravitational waves and black hole mergers as part of the Laser Interferometer Gravitational-Wave Observatory (LIGO) - but also other internationally significant research from the Department of Physics. Discover why Strathclyde's physics research is making ripples...

Strathprints also exposes world leading research from the Faculties of Science, Engineering, Humanities & Social Sciences, and from the Strathclyde Business School.

Discover more...

On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin

Rowan, E.G. and Pemberton, K.E. and Harvey, Alan L. (1990) On the blockade of acetylcholine release at mouse motor nerve terminals by beta-bungarotoxin and crotoxin. British Journal of Pharmacology, 100 (2). pp. 301-304. ISSN 0007-1188

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

Abstract

1. beta-Bungarotoxin and crotoxin are phospholipose A2 neurotoxins, which block irreversibly the evoked release of acetylcholine from motor nerve terminals of mouse triangularis sterni preparations. 2. Extracellular recording of nerve terminal action potentials reveal that inhibition of transmitter release is not associated with failure of the action potential to invade nerve terminals. 3. When evoked transmitter release (measured as intracellularly recorded endplate potentials) was blocked by beta-bungarotoxin, spontaneous acetylcholine release was stimulated as in control experiments by K(+)-induced depolarization and by the Ca2(+)-ionophore A23187. 4. The site of action of the toxins remains to be elucidated but would appear to be associated with the coupling of action potential induced-depolarization to the release mechanism, rather than with the release mechanism itself.