| First Author | Shiraiwa T | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 355 |
| Issue | 4 | Pages | 1019-24 |
| PubMed ID | 17335778 | Mgi Jnum | J:120329 |
| Mgi Id | MGI:3706281 | Doi | 10.1016/j.bbrc.2007.02.063 |
| Citation | Shiraiwa T, et al. (2007) Involvement of the calcium channel beta3 subunit in olfactory signal transduction. Biochem Biophys Res Commun 355(4):1019-24 |
| abstractText | 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 beta3-deficient mice. RT-PCR and Western blots confirmed the expression of various types of Ca2+ channels in the nasal turbinate. Electrophysiological evaluations revealed that beta3-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 beta3-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 omega-conotoxin GVIA in the electro-olfactogram. Diluted male urine odors induced higher Fos immunoreactivity in the main olfactory bulbs of beta3-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 beta3 subunit in olfactory signal transduction. |
