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...

Neurotoxicity of ammodytoxin A in the envenoming bites of vipera ammodytes ammodytes

Logonder, U. and Krizaj, I. and Rowan, E.G. and Harris, J.B. (2008) Neurotoxicity of ammodytoxin A in the envenoming bites of vipera ammodytes ammodytes. Journal of Neuropathology and Experimental Neurology, 67 (10). pp. 1011-1019. ISSN 0022-3069

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

Abstract

Envenoming bites by Vipera ammodytes ammodytes (the long-nosed viper) can cause life-threatening neurotoxicity, particularly in children. We investigated the mechanisms of the neurotoxicity of ammodytoxin A, the principal toxin in the venom of these snakes, in isolated nerve-muscle preparations from mice. The toxin was bound selectively to the neuromuscular junction, and at concentrations similar to those likely to be found in the circulation of young bite victims, it blocked the response of the muscle to indirect but not direct stimulation. Electron microscopy showed that the toxin induced a small but insignificant depletion of synaptic vesicles from motor nerve terminals; nerve terminal mitochondria were swollen and damaged, but plasma membranes of terminal boutons were undamaged. Exposure to the toxin did not affect postjunctional acetylcholine receptors or cause structural damage to preterminal motor axons or muscle fibers. Spontaneous transmitter release was similarly unaffected. Taken together, these results indicate that ammodytoxin A is the principal agent involved in the neurotoxic activity of the venom of V ammodytes ammodytes and that the underlying cause of the failure of transmission may be the deenergization of the nerve terminal resulting from mitochondrial degeneration and subsequent impairment of coupling between the action-potential-induced depolarization of the nerve terminal and the evoked transmitter release. (C) 2008 American Association of Neuropathologists, Inc