Deficits in responding to brief noise offsets in Kcna1 -/- mice reveal a contribution of this gene to precise temporal processing seen previously only for stimulus onsets.

The voltage-gated potassium channel subunit Kv1.1 encoded by the Kcna1 gene is expressed in many brainstem nuclei, and electrophysiological studies of Kcna1-null mutant (-/-) single neurons suggest that channels containing this subunit are critical for precise processing of rapid acoustic perturbations. We tested the hypothesis that brief offsets of a background noise are behaviorally less salient for Kcna1 -/- mice, measured by changes in noise offset inhibition of acoustic startle reflexes (ASR). In experiment 1, noise offset was followed by ASR-eliciting sound bursts either after 1-10 ms quiet intervals or after the return of noise for 10-290 ms following 10-ms quiet gaps. ASR inhibition to offset and gaps was initially higher in +/+ mice but persisted longer in -/- mice. Experiment 2 contrasted brief abrupt offsets with ramped offsets of the same duration up to 10 ms, the ramps intended to simulate progressively slower internal decays of afferent processing. Both groups had greater inhibition for abrupt offsets at asymptote, and this difference was evident at the 1-ms interval in +/+ but not -/- mice. Further, the asymptotic effect of ramped offsets in +/+ mice was equal to that produced by abrupt offsets in null mutants, suggesting more perseveration of internal afferent activity following noise offset in -/- mice. Overall, these data are consistent with prior electrophysiological studies showing that the neural mechanisms for processing acoustic transients are less effective in Kcna1 -/- mice and support previous proposals that Kv1.1 contributes to the perception of animal vocalizations and human speech.