Spontaneous spiking and synaptic depression underlie noradrenergic control of feed-forward inhibition.
Spontaneous spiking and synaptic depression underlie noradrenergic control of feed-forward inhibition.
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DOI：
10.1016/j.neuron.2011.05.039
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发表时间：
2011-07-28
期刊：
影响因子：
16.2
通讯作者：
Trussell LO
中科院分区：
文献类型：
--
作者：
Kuo SP;Trussell LO
即使在没有外部刺激的情况下，跨越不同大脑区域的抑制性中间神经元也通常表现出自发的尖峰活动。如何将刺激诱发的抑制与自发放电引起的背景抑制区分开来，目前尚不清楚。我们发现去甲肾上腺素同时减少自发抑制输入，增强小鼠耳蜗背核（DCN）主要神经元的诱发抑制电流。总之，这些效应产生了刺激诱发抑制的信噪比的大幅增加。令人惊讶的是，背景电流和诱发电流的相反作用都可以归因于甘氨酸能中间神经元自发尖峰的去甲肾上腺素能沉默。在自发放电过程中，甘氨酸的释放由于强烈的短期抑制而减少。背景峰的消除减轻了抑制性突触的抑郁，从而增强了刺激诱发的抑制。我们的发现说明了一种简单而强大的神经调节机制来改变背景和刺激诱发信号之间的平衡。
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.
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影响因子：
16.2
作者：
Bender, Kevin J.;Ford, Christopher P.;Trussell, Laurence O.
通讯作者：
Trussell, Laurence O.
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作者：
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