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1 Neurobiology and Behavior Program, University of Washingon, Seattle, Washington, United States; Departments of Otolaryngology-HNS and Pharmacology, University of Washington, Seattle, Washington, United States; The Virginia Merrill Bloedel Hearing Research Center, University of Washington, Seattle, Washington, United States
* To whom correspondence should be addressed. E-mail: bltempel{at}u.washington.edu.
Low-threshold, voltage-gated potassium currents (Ikl) are widely expressed in auditory neurons that can fire temporally precise action potentials (APs). In the medial nucleus of the trapezoid body, channels containing the Kv1.1 subunit (encoded by the Kcna1 gene) underlie Ikl. Using pharmacology, genetics and whole-cell patch-clamp recordings in mouse brain slice, we tested the role of Ikl in limiting AP latency-variability (jitter) in response to trains of single inputs at moderate to high rates. With dendrotoxin-K (DTX-K, which selectively blocks Kv1.1 containing channels), we blocked Ikl maximally (
80% with 100 nM DTX-K) or partially ( 50% with one hour incubation in 3 nM DTX-K). Ikl was similar in 3 nM DTX-K-treated cells and cells from Kcna1-/- mice, allowing a comparison of these two different methods of Ikl reduction. In response to current injection, Ikl reduction increased the temporal window for AP initiation, and increased jitter in response to the smallest currents that were able to drive APs. While 100 nM DTX-K caused the largest increases, latency and jitter in cna1-/- and 3 nM DTX-K-treated cells were similar to each other, but increased compared to +/+. The near-phenocopy of the Kcna1-/- with 3 nM DTX-K demonstrates that acute blockade of a subset of the Kv1.1 containing channels is functionally similar to the chronic elimination of all Kv1.1 subunits. During rapid stimulation (100-500 Hz), Ikl reduction increased jitter in response to both large and small inputs. These data show Ikl is critical for maintaining AP temporal precision at physiologically relevant firing rates.
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