| First Author | Fadool DA | Year | 2004 |
| Journal | Neuron | Volume | 41 |
| Issue | 3 | Pages | 389-404 |
| PubMed ID | 14766178 | Mgi Jnum | J:87813 |
| Mgi Id | MGI:3028258 | Doi | 10.1016/s0896-6273(03)00844-4 |
| Citation | Fadool DA, et al. (2004) Kv1.3 channel gene-targeted deletion produces 'Super-Smeller Mice' with altered glomeruli, interacting scaffolding proteins, and biophysics. Neuron 41(3):389-404 |
| abstractText | Mice with gene-targeted deletion of the Kv1.3 channel were generated to study its role in olfactory function. Potassium currents in olfactory bulb mitral cells from Kv1.3 null mice have slow inactivation kinetics, a modified voltage dependence, and a dampened C-type inactivation and fail to be modulated by activators of receptor tyrosine signaling cascades. Kv1.3 deletion increases expression of scaffolding proteins that normally regulate the channel through protein-protein interactions. Kv1.3-/- mice have a 1,000- to 10,000-fold lower threshold for detection of odors and an increased ability to discriminate between odorants. In accordance with this heightened sense of smell, Kv1.3-/- mice have glomeruli or olfactory coding units that are smaller and more numerous than those of wild-type mice. These data suggest that Kv1.3 plays a far more reaching role in signal transduction, development, and olfactory coding than that of the classically defined role of a potassium channel-to shape excitability by influencing membrane potential. |
