Evidence for a neurotoxic activity in crude venom of the stonefish (Synanceia verrucosa)

The neurotoxic effects of the Synanceia verrucosa venom were investigated in rodents. After intracranial injection in mice (50-125 ng/g), venom induced constant symptoms such as ataxia, circling, partial or complete reversible limbs paralysis, scratching, rolling, sleep-like periods and violent clon...

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Bibliographic Details
Published inJournal of natural toxins Vol. 11; no. 4; p. 305
Main Authors Breton, Patrick, Delamanche, Iroudayanadin, Buée, Janine, Goudey-Perriére, Françoise, Perriére, Claude
Format Journal Article
LanguageEnglish
Published United States 01.12.2002
Subjects
Animals
Brain - drug effects
Brain - pathology
Electroencephalography
Fish Venoms - isolation & purification
Fish Venoms - toxicity
Fishes, Poisonous
Glycoproteins - isolation & purification
Glycoproteins - toxicity
Injections, Intraventricular
Lethal Dose 50
Male
Mice
Mice, Inbred Strains
Neurotoxicity Syndromes - pathology
Neurotoxicity Syndromes - physiopathology
Rats
Rats, Wistar
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Summary:The neurotoxic effects of the Synanceia verrucosa venom were investigated in rodents. After intracranial injection in mice (50-125 ng/g), venom induced constant symptoms such as ataxia, circling, partial or complete reversible limbs paralysis, scratching, rolling, sleep-like periods and violent clonic seizure conducing in few seconds to death. EEG alterations occurring in rat brain after intracerebroventricular injection (50-100 microg) were precised. An initial phase was characterized by short repetitive tonic seizure periods together with a significant rise of the relative power in the delta band, no significant modification of the theta II rhythm (4-7 Hz), a decreasing of energy in theta I (7-12 Hz) and 15-40 Hz bands. A second phase was characterized by a marked generalized slowing with transient drastic decreasing of the amplitude and flattening of cortical EEG (comatose state) as the main elements. Propanolol did not reverse the EEG effects of the venom except a slight decrease of the slow wave amplitude. Previous intracerebroventricular administration of a K+(ATP) blocker generally decrease the delay of death. Histopathologic examination of the brain of surviving animals did not reveal any microscopic lesions. These results suggest (1) a complex mechanism of the venom in its neuropathologic expression; (2) at the doses tested, symptoms are not related to adrenergic pathways, K+(ATP) channel opener (verrucotoxin) is not implied in the neurotoxic effect, and the effect of the venom, which not affecting the theta II rhythm, seemed not to be exerted through cholinergic pathway.
ISSN:1058-8108