Intracellular recordings reveal novel features of neurons that code interaural intensity disparities in the inferior colliculus.

Intracellular recordings reveal novel features of neurons that code interaural intensity disparities in the inferior colliculus.
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DOI:
10.1523/jneurosci.2228-10.2010
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发表时间:
2010-10-27
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Pollak GD
Pollak GD
中科院分区:
其他
文献类型:
--
作者:
Li N;Gittelman JX;Pollak GD

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下丘(IC)的许多细胞被对侧刺激所兴奋,被同侧刺激所抑制,并且被认为是声音定位的重要因素。这些兴奋抑制(EI)细胞包括一个不同的群体,即使他们表现出共同的双耳响应特性。以前的细胞外研究表明,不同的电路,产生相同的EI性能之间的IC人口的多样性结果,其中一些继承的属性从较低的核,一些是从头形成的IC,而其他继承的EI功能,抑制电路修改。在这里,我们评估了差分电路记录输入(突触后电位)和输出(尖峰)与在体内全细胞记录清醒的墨西哥自由尾蝙蝠的IC。我们发现,少数EI细胞要么继承其双耳属性从较低的双耳核或EI属性创建在IC通过抑制性预测从同侧耳,功能与细胞外研究中观察到的一致。然而,在大多数的EI细胞同侧信号诱发阈下EPSP表现矛盾的EPSP振幅随强度增加,即使双耳信号具有相同的同侧强度产生逐步更大的尖峰supplies。我们提出的电路,可以解释我们观察到的反应,并建议同侧诱发的EPSPs可以影响IC细胞的动态信号与耳间强度差异,随着时间的推移而变化,如移动声源或多个声音,发生在复杂的声学环境的反应。
Many cells in the inferior colliculus (IC) are excited by contralateral and inhibited by ipsilateral stimulation and are thought to be important for sound localization. These excitatory-inhibitory (EI) cells comprise a diverse group, even though they exhibit a common binaural response property. Previous extracellular studies showed the diversity results from different circuits that generate the same EI property among the IC population, where some inherit the property from a lower nucleus, some are formed de novo in the IC whereas others inherit EI features that are modified by inhibitory circuits. Here we evaluated the differential circuitry by recording inputs (postsynaptic potentials) and outputs (spikes) with in vivo whole cell recordings from the IC of awake Mexican free tailed bats. We show that a minority of EI cells either inherited their binaural property from a lower binaural nucleus or the EI property was created in the IC via inhibitory projections from the ipsilateral ear, features consistent with those observed in extracellular studies. However, in a majority of EI cells ipsilateral signals evoked subthreshold EPSPs that behaved paradoxically in that EPSP amplitudes increased with intensity, even though binaural signals with the same ipsilateral intensities generated progressively greater spike suppressions. We propose circuitry that can account for the responses we observed and suggest that the ipsilaterally evoked EPSPs could influence the responsiveness of IC cells to dynamic signals with interaural intensity disparities that change over time, such as moving sound sources or multiple sounds that occur in complex acoustic environments.