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Eur J Pharmacol. 2000 Sep 15;404(1-2):79-88.

Rabies virus infection prevents the modulation by alpha(2)-adrenoceptors, but not muscarinic receptors, of Ca(2+) channels in NG108-15 cells.

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Laboratory of Pharmacology, Department of Veterinary Science, Faculty of Agriculture, Gifu University, 1-1 Yanagido, 501-1193, Gifu, Japan.


In mouse neuroblastoma x rat glioma hybrid (NG108-15) cells, we examined whether rabies virus infection affects the voltage-dependent Ca(2+) current (I(Ca)) and agonist-induced I(Ca) inhibition. The viral infection had little effect on the current-voltage relationship for peak I(Ca) or on the late I(Ca) that remained at the end of a 200-ms step depolarization. Noradrenaline and carbachol, via alpha(2)-adrenoceptors and muscarinic receptors, respectively, reduced I(Ca) concentration dependently. The maximum effect of noradrenaline was attained at 10 microM with 19.4+/-1.8% inhibition of I(Ca), which was significantly decreased to 9.9+/-1.3% after viral infection. The decrease was not reversed with 100 microM noradrenaline, suggesting that it does not result from a decrease in agonist sensitivity of cells. The maximum effect of carbachol (300 microM; 27.7+/-2.9% inhibition) remained unchanged, despite carbachol sharing intracellular signaling pathways with noradrenaline. These results indicate that in NG108-15 cells, rabies virus infection does not alter the functional expression of voltage-dependent Ca(2+) channels, but it attenuates the alpha(2)-adrenoceptor-mediated I(Ca) inhibition, possibly through some change at the receptor level.

[Indexed for MEDLINE]

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