Selective cytostatic and neurotoxic effects of avermectins and activation of the GABAalpha receptors

A natural avermectin complex, aversectin C, was shown to be capable of exerting selective cytostatic and neurotoxic effects on mammalian cells. Specifically, it killed proliferating neuroblastoma B103 cells but was non-toxic for differentiated cells of this culture. The antiproliferation action of a...

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Bibliographic Details
Published inBioscience reports Vol. 19; no. 6; p. 535
Main Authors Kokoz, Y M, Tsyganova, V G, Korystova, A F, Grichenko, A S, Zenchenko, K I, Drinyaev, V A, Mosin, V A, Kruglyak, E B, Sterlina, T S, Victorov, A V
Format Journal Article
LanguageEnglish
Published England 01.12.1999
Subjects
Animals
Bicuculline - pharmacology
Cell Differentiation - drug effects
Cell Division - drug effects
Dose-Response Relationship, Drug
GABA Agonists - pharmacology
GABA Antagonists - pharmacology
Ivermectin - analogs & derivatives
Ivermectin - pharmacology
Male
Neuroblastoma - drug therapy
Neurons - drug effects
Neurotoxins - pharmacology
Pentobarbital - pharmacology
Picrotoxin
Rats
Rats, Wistar
Receptors, GABA-A - drug effects
Septal Nuclei - drug effects
Tumor Cells, Cultured
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Summary:A natural avermectin complex, aversectin C, was shown to be capable of exerting selective cytostatic and neurotoxic effects on mammalian cells. Specifically, it killed proliferating neuroblastoma B103 cells but was non-toxic for differentiated cells of this culture. The antiproliferation action of aversectin C was not inhibited by bicuculline or picrotoxin, antagonists of the GABAalpha receptors, and was partly due to the action of avermectin A1, a component of aversectin C. Aversectin C irreversibly suppressed activity of 60% neurons in medial septal slices of the rat brain. More than 55% of them were the GABAalpha- and B1-sensitive neurons whereas the rest, about 45% neurons, were the GABAalpha-insensitive and the neurotoxic effect of aversectin C was caused mainly by the B2 component.
ISSN:0144-8463