Abstract
Despite the expression of voltage-dependent Ca2+ channels in nasal turbinate epithelium, their role in odorant chemosensation has remained obscure. Therefore, we investigated olfactory neurotransduction in β3-deficient mice. RT-PCR and Western blots confirmed the expression of various types of Ca2+ channels in the nasal turbinate. Electrophysiological evaluations revealed that β3-null mice had a 60% reduction in the high-voltage-dependent Ca2+ currents in olfactory receptor neurons due to reduced N- and L-type channel currents. The β3-null mice showed increased olfactory neuronal activity to triethylamine, and this effect was mimicked by the perfusion of the specific N-type Ca2+ channel inhibitor ω-conotoxin GVIA in the electro-olfactogram. Diluted male urine odors induced higher Fos immunoreactivity in the main olfactory bulbs of β3-deficient mice, indicating enhanced signal transduction of odor information in these mice. Our data indicate the involvement of voltage-dependent Ca2+ channels and importance of the β3 subunit in olfactory signal transduction.
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