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
E-mail: es@obihiro.ac.jp
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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