| First Author | Allen PD | Year | 2008 |
| Journal | Hear Res | Volume | 246 |
| Issue | 1-2 | Pages | 52-8 |
| PubMed ID | 18926893 | Mgi Jnum | J:143590 |
| Mgi Id | MGI:3828218 | Doi | 10.1016/j.heares.2008.09.009 |
| Citation | Allen PD, et al. (2008) Kv1.1 channel subunits are not necessary for high temporal acuity in behavioral and electrophysiological gap detection. Hear Res 246(1-2):52-58 |
| abstractText | The Kv1.1 potassium channel subunit, encoded by the Kcna1 gene, is heavily expressed in the auditory brainstem and is thought to have a critical role in producing the high temporal precision of action potentials characteristic of the auditory system. Our intent was to determine whether temporal acuity was reduced in Kcna1 null-mutant (-/-) mice, compared to wild-type (+/+) and heterozygotic mice (+/-), as measured by the encoding of gaps in the inferior colliculus by near-field auditory evoked potentials (NFAEP) or behavioral gap detection (BGD) using a prepulse inhibition paradigm. NFAEPs were collected at 40, 60 and 80dB SPL with gap durations from 0.5 to 64ms. BGD data were collected using silent gaps in 70dB noise from 1 to 15 ms in duration. There were no systematic effects of Kcna1 genotype on NFAEP recovery functions, NFAEP latencies, or the time constant for BGD, but there was a small reduction in asymptotic prepulse inhibition for the longest gap stimuli in -/- mice. Gap thresholds were approximately 1-2ms across genotypes, stimulus conditions, and paradigms. These data suggest that the neural pathways encoding behaviorally relevant, rapid auditory temporal fluctuations are not limited by the absence of Kv1.1 expression. |
