Eiki Satoh*, Toshiaki Ishii and Masakazu Nishimura
Department of Pharmacology, University of Obihiro School of Veterinary Medicine, Obihiro 080-8555, Japan
*Corresponding author. FAX: +81-155-49-5402
Abstract: The present study was conducted to elucidate the mechanism of the maitotoxin (MTX)-induced increase in intrasynaptosomal free calcium level ([Ca2+]i). The MTX (1 ng/ml)-induced increase in [Ca2+]i was partially inhibited by the omission of extracellular Ca2+ (Ca 2+e) or the addition of verapamil, but not by adding nifedipine, w-agatoxin IVA, w-conotoxin GVIA and w-conotoxin MVIIC. An increase in [Ca2+]i in the absence of Ca2+e was sensitive to procaine, TMB-8, genistein and verapamil, but not to ryanodine and U-73122. These results may suggest that MTX increases [Ca2+]i by stimulating Ca2+ entry through voltage-independent nonselective cation channels and Ca2+ release from stores through a phospholipase C-g1-mediated pathway in rat cerebrocortical synaptosomes.
Keywords: Maitotoxin, Synaptosomes, Cytosolic free calcium
Copyright The Japanese Pharmacological Society
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