ToxSci Advance Access published online on December 1, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfj064
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1 Biochemistry and Molecular Biology Department, Institute of Biotechnology, University of Oviedo, Oviedo, Spain
* To whom correspondence should be addressed. Yessotoxin (YTX) and its analogues are disulphated polyether compounds of increasing occurrence in seafood. The biological effects of these algal toxins on mammals and the risk associated to their ingestion have not been clearly established. We have used primary cultures of rat cerebellar neurons to investigate whether YTX affected survival and functioning of central nervous system neurons. Exposure to YTX (
Received October 6, 2005
Accepted November 23, 2005
Neurotoxicology
Potent Neurotoxic Action of the Shellfish Biotoxin Yessotoxin on Cultured Cerebellar Neurons
Anabel Pérez-Gómez 1,
Amaia Ferrero-Gutierrez 2,
Antonello Novelli 2,
José M. Franco 3,
Beatriz Paz 3,
and
M. Teresa Fernández-Sánchez 1 *
2 Biochemistry and Molecular Biology Department, Institute of Biotechnology, University of Oviedo, Oviedo, Spain; Psychology Department, Institute of Biotechnology, University of Oviedo, Oviedo, Spain
3 Toxic Fitoplancton Associated Unit (CSIC-IEO), Spanish Institute of Oceanography, Oceanographic Center, Box 1552, 36200 Vigo, Spain
M. Teresa Fernández-Sánchez, E-mail: mfernandez{at}bioquimica.uniovi.es
Abstract 
25nM) caused first (
8h) weakening, granulation and fragmentation of neuronal network, and later (48h) complete disintegration of neurites and extensive neuronal death, with a significant decrease in the amount of filamentous actin. The concentration of YTX that reduced by 50% the maximum neuronal survival (EC5048) was 20nM. Lower toxin concentrations (15 nM) also caused visible signs of toxicity affecting neuronal network primarily. Removal of YTX after 5h exposure delayed the onset of neurotoxicity but did not prevent neuronal degeneration and death. YTX induced a 2- fold increase in cytosolic calcium that was prevented by the voltage-sensitive calcium channel antagonists nifedipine and verapamil. These antagonists were, however, completely ineffective in reducing neurotoxicity. Voltage-sensitive sodium channel antagonists saxitoxin and nefopam, and the NMDA receptor antagonist MK-801 also failed to prevent YTX neurotoxicity. Neuronal death by YTX involved typical hallmarks of apoptosis and required the synthesis of new proteins. Our data suggest neuronal tissue to be a vulnerable biological target for YTX. The potent neurotoxicity of YTX we report raise reasonable concern about the potential risk that exposure to YTX may represent for neuronal survival in vivo.
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