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.
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.
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Kcna1 -/- 小鼠对短暂噪声偏移的反应缺陷揭示了该基因对以前仅针对刺激开始时所见的精确时间处理的贡献。
DOI：
10.1007/s10162-011-0312-1
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发表时间：
2012
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影响因子：
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通讯作者：
Allen,PaulD
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文献类型：
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作者：
Ison,JamesR;Allen,PaulD
kcna1基因编码的电压门控钾通道亚基Kv1.1在许多脑干核中表达，对kcna1缺失突变（−/−）单个神经元的电生理研究表明，含有该亚基的通道对于快速声扰动的精确处理至关重要。我们通过噪声抵消对声惊吓反射（ASR）抑制的变化来测试背景噪声的短暂偏移对forKcna1 - / -小鼠的行为不太显著的假设。在实验1中，在噪声抵消之后，在安静间隔1 - 10ms或在安静间隔10ms后10-290 ms的噪音返回后，出现asr引发的声音爆发。ASR对抵消和间隙的抑制作用在+/+小鼠中最初较高，但在−/−小鼠中持续时间更长。实验2对比了短暂的突然偏移和持续时间长达10 ms的斜坡偏移，斜坡旨在模拟传入处理的逐渐缓慢的内部衰减。两组在渐近线处对突然偏移有更大的抑制作用，在+/+小鼠中，这种差异在1 ms间隔内很明显，而在−/−小鼠中则没有。此外，在+/+小鼠中，倾斜偏移的渐近效应与零突变体中突然偏移产生的渐近效应相等，这表明在−/−小鼠中，噪声偏移后内部传入活动的持久性更强。总的来说，这些数据与先前的电生理学研究一致，表明inKcna1 - / -小鼠处理声瞬态的神经机制不太有效，并支持了先前关于Kv1.1有助于动物发声和人类语言感知的建议。
The voltage-gated potassium channel subunit Kv1.1 encoded by theKcna1gene is expressed in many brainstem nuclei, and electrophysiological studies ofKcna1-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 forKcna1−/− 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 inKcna1−/− mice and support previous proposals that Kv1.1 contributes to the perception of animal vocalizations and human speech.