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长期高强度声音刺激抑制 CA1 锥体神经元中的 h 电流 (I ) 。

Long-term high-intensity sound stimulation inhibits h current (I ) in CA1 pyramidal neurons.

机构信息

Department of Physiology, FMRP, University of São Paulo, Ribeirão Preto, SP, Brazil.

Department of Physics, FFCLRP, University of São Paulo, Ribeirão Preto, SP, Brazil.

出版信息

Eur J Neurosci. 2018 Jun;47(11):1401-1413. doi: 10.1111/ejn.13954. Epub 2018 Jun 4.

DOI:10.1111/ejn.13954
PMID:29779233
Abstract

Afferent neurotransmission to hippocampal pyramidal cells can lead to long-term changes to their intrinsic membrane properties and affect many ion currents. One of the most plastic neuronal currents is the hyperpolarization-activated cationic current (I ), which changes in CA1 pyramidal cells in response to many types of physiological and pathological processes, including auditory stimulation. Recently, we demonstrated that long-term potentiation (LTP) in rat hippocampal Schaffer-CA1 synapses is depressed by high-intensity sound stimulation. Here, we investigated whether a long-term high-intensity sound stimulation could affect intrinsic membrane properties of rat CA1 pyramidal neurons. Our results showed that I is depressed by long-term high-intensity sound exposure (1 min of 110 dB sound, applied two times per day for 10 days). This resulted in a decreased resting membrane potential, increased membrane input resistance and time constant, and decreased action potential threshold. In addition, CA1 pyramidal neurons from sound-exposed animals fired more action potentials than neurons from control animals; however, this effect was not caused by a decreased I . On the other hand, a single episode (1 min) of 110 dB sound stimulation which also inhibits hippocampal LTP did not affect I and firing in pyramidal neurons, suggesting that effects on I are long-term responses to high-intensity sound exposure. Our results show that prolonged exposure to high-intensity sound affects intrinsic membrane properties of hippocampal pyramidal neurons, mainly by decreasing the amplitude of I .

摘要

传入到海马锥体细胞的神经传递会导致其内在膜特性的长期变化,并影响多种离子电流。其中最具可塑性的神经元电流之一是超极化激活阳离子电流(I h),它会响应多种生理和病理过程(包括听觉刺激)而在 CA1 锥体细胞中发生变化。最近,我们证明了大鼠海马 Schaffer-CA1 突触中的长时程增强(LTP)会被高强度声音刺激所抑制。在这里,我们研究了长期高强度声音刺激是否会影响大鼠 CA1 锥体神经元的内在膜特性。我们的结果表明,长期高强度声音暴露(每天两次,每次 1 分钟,强度为 110dB 的声音,持续 10 天)会抑制 Ih。这导致了静息膜电位降低、膜输入电阻和时间常数增加以及动作电位阈值降低。此外,来自声音暴露动物的 CA1 锥体神经元比来自对照动物的神经元发出更多的动作电位;然而,这种效应不是由 Ih 减少引起的。另一方面,单次(1 分钟)110dB 声音刺激也会抑制海马 LTP,但不会影响 Ih 和锥体神经元的放电,这表明 Ih 的变化是对高强度声音暴露的长期反应。我们的结果表明,长时间暴露于高强度声音会影响海马锥体神经元的内在膜特性,主要通过降低 Ih 的幅度来实现。

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