title: Decreased temporal precision of auditory signaling in Kcna1-null mice: an electrophysiological study in vivo.
abstract: The voltage-gated potassium (Kv) channel subunit Kv1.1, encoded by the Kcna1 gene, is expressed strongly in the ventral cochlear nucleus (VCN) and the medial nucleus of the trapezoid body (MNTB) of the auditory pathway. To examine the contribution of the Kv1.1 subunit to the processing of auditory information, in vivo single-unit recordings were made from VCN neurons (bushy cells), axonal endings of bushy cells at MNTB cells (calyces of Held), and MNTB neurons of Kcna1-null (-/-) mice and littermate control (+/+) mice. Thresholds and spontaneous firing rates of VCN and MNTB neurons were not different between genotypes. At higher sound intensities, however, evoked firing rates of VCN and MNTB neurons were significantly lower in -/- mice than +/+ mice. The SD of the first-spike latency (jitter) was increased in VCN neurons, calyces, and MNTB neurons of -/- mice compared with +/+ controls. Comparison along the ascending pathway suggests that the increased jitter found in -/- MNTB responses arises mostly in the axons of VCN bushy cells and/or their calyceal terminals rather than in the MNTB neurons themselves. At high rates of sinusoidal amplitude modulations, -/- MNTB neurons maintained high vector strength values but discharged on significantly fewer cycles of the amplitude-modulated stimulus than +/+ MNTB neurons. These results indicate that in Kcna1-null mice the absence of the Kv1.1 subunit results in a loss of temporal fidelity (increased jitter) and the failure to follow high-frequency amplitude-modulated sound stimulation in vivo.
authors.affiliation: University of Washington, V. M. Bloedel Hearing Research Center and Department of Otolaryngology, Seattle, Washington 98195, USA. connyks@u.washington.edu
authors.forename: Cornelia
authors.initials: C
authors.lastname: Kopp-Scheinpflug
authors.forename: Katja
authors.initials: K
authors.lastname: Fuchs
authors.forename: William R
authors.initials: WR
authors.lastname: Lippe
authors.forename: Bruce L
authors.initials: BL
authors.lastname: Tempel
authors.forename: Rudolf
authors.initials: R
authors.lastname: Rübsamen
mesh_terms: D000161:Acoustic Stimulation / Q000379:methods; D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001306:Auditory Pathways / Q000502:physiology*; D001309:Auditory Threshold; D017626:Cochlear Nucleus / Q000502:physiology; D004567:Electrodes, Implanted; D004594:Electrophysiology; D051662:Kv1.1 Potassium Channel; D051379:Mice; D018345:Mice, Knockout; D015221:Potassium Channels / Q000172:deficiency* / Q000235:genetics; D024642:Potassium Channels, Voltage-Gated; D011930:Reaction Time / Q000235:genetics / Q000502:physiology*; D013997:Time Factors
chemical_list: C496947:Kcna1 protein, mouse; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D051662:Kv1.1 Potassium Channel