Kv1.3 Channel Gene-Targeted Deletion Produces "Super-Smeller Mice" with Altered Glomeruli, Interacting Scaffolding Proteins, and Biophysics

D. A. Fadool, K. Tucker, R. Perkins, G. Fasciani, R. N. Thompson, A. D. Parsons, J. M. Overton, P. A. Koni, R. A. Flavell, L. K. Kaczmarek

Research output: Contribution to journalArticlepeer-review

116 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)389-404
Number of pages16
JournalNeuron
Volume41
Issue number3
DOIs
StatePublished - Feb 5 2004

ASJC Scopus subject areas

  • Neuroscience(all)

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