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首页> 外文期刊>Neuron >Spontaneous spiking and synaptic depression underlie noradrenergic control of feed-forward inhibition.
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Spontaneous spiking and synaptic depression underlie noradrenergic control of feed-forward inhibition.

机译：自发的尖峰和突触抑制是前馈抑制的去甲肾上腺素能控制的基础。

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摘要

Inhibitory interneurons across diverse brain regions commonly exhibit spontaneous spiking activity, even in the absence of external stimuli. It is not well understood how stimulus-evoked inhibition can be distinguished from background inhibition arising from spontaneous firing. We found that noradrenaline simultaneously reduced spontaneous inhibitory inputs and enhanced evoked inhibitory currents recorded from principal neurons of the mouse dorsal cochlear nucleus (DCN). Together, these effects produced a large increase in signal-to-noise ratio for stimulus-evoked inhibition. Surprisingly, the opposing effects on background and evoked currents could both be attributed to noradrenergic silencing of spontaneous spiking in glycinergic interneurons. During spontaneous firing, glycine release was decreased due to strong short-term depression. Elimination of background spiking relieved inhibitory synapses from depression and thereby enhanced stimulus-evoked inhibition. Our findings illustrate a simple yet powerful neuromodulatory mechanism to shift the balance between background and stimulus-evoked signals.
机译：即使在没有外部刺激的情况下，跨不同大脑区域的抑制性中间神经通常也表现出自发的尖峰活动。尚不清楚如何将刺激诱发的抑制与自发激发产生的背景抑制区分开。我们发现去甲肾上腺素同时减少自小鼠背侧耳蜗核（DCN）的主要神经元记录的自发抑制输入和增强诱发的抑制电流。在一起，这些效应使刺激引起的抑制的信噪比大大增加。出乎意料的是，对本底和诱发电流的相反影响都可归因于甘氨酸能中神经元自发突触的去甲肾上腺素能沉默。在自发放电期间，由于强烈的短期抑制作用，甘氨酸的释放减少。消除背景尖峰可减轻抑郁症的抑制突触，从而增强刺激诱发的抑制作用。我们的发现说明了一种简单而强大的神经调节机制，可以改变背景信号和刺激信号之间的平衡。

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