Sensory deprivation regulates the development of the hyperpolarization-activated current in auditory brainstem neurons
Sensory deprivation regulates the development of the hyperpolarization-activated current in auditory brainstem neurons
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DOI：
10.1111/j.1460-9568.2009.06925.x
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发表时间：
2009-10-01
影响因子：
3.4
通讯作者：
Koch, Ursula
中科院分区：
文献类型：
--
作者：
Hassfurth, Benjamin;Magnusson, Anna K.;Koch, Ursula
超极化激活和环核苷酸门控(HCN)通道在上橄榄复合体中高度表达，上橄榄复合体是双耳信息处理的主要部位。这种超极化激活电流(i-h)调节神经元的兴奋性，并增强对双耳声学提示的时间精确度分析。采用全细胞膜片钳技术，观察了大鼠外侧上橄榄核(LSO)和斜方体内侧核(MNTB)神经元在听力开始前后的I-h电流特性。此外，我们还验证了这样一种假设，即i-h电流是由感觉输入活动主动调节的，在听力发作前进行双侧和单侧耳蜗区消融，从而导致慢性听觉剥夺。结果表明，听觉发作后，LSO神经元的I-h电流迅速升高，而MNTB神经元的I-h电流变化不大。我们还发现LSO和MNTB在成熟期动物的最大电流密度、电压依赖性和激活时间常数上存在显著差异。在听力开始前双侧耳蜗术后，LSO的I-h电流增大，MNTB的I-h电流减小。因此，在LSO中，这导致了这些神经元的去极化静息膜电位和较低的输入电阻。因此，这种依赖于活动的动态平衡变化可能会导致对剩余输入的反应增强。
Hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels are highly expressed in the superior olivary complex, the primary locus for binaural information processing. This hyperpolarization-activated current (I-h) regulates the excitability of neurons and enhances the temporally precise analysis of the binaural acoustic cues. By using the whole-cell patch-clamp technique, we examined the properties of I-h current in neurons of the lateral superior olive (LSO) and the medial nucleus of the trapezoid body (MNTB) before and after hearing onset. Moreover, we tested the hypothesis that I-h currents are actively regulated by sensory input activity by performing bilateral and unilateral cochlear ablations before hearing onset, resulting in a chronic auditory deprivation. The results show that after hearing onset, I-h currents are rapidly upregulated in LSO neurons, but change only marginally in neurons of the MNTB. We also found a striking difference in maximal current density, voltage dependence and activation time constant between the LSO and the MNTB in mature-like animals. Following bilateral cochlear ablations before hearing onset, the I-h currents were scaled up in the LSO and scaled down in the MNTB. Consequently, in the LSO this resulted in a depolarized resting membrane potential and a lower input resistance of these neurons. This type of activity-dependent homeostatic change could thus result in an augmented response to the remaining inputs.