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视觉皮层中血清素能传入对持续活动和诱发活动的可分离增益控制。

Separable gain control of ongoing and evoked activity in the visual cortex by serotonergic input.

机构信息

Optical Imaging Group, Institut für Neuroinformatik, Ruhr University Bochum, Bochum, Germany.

International Graduate School of Neuroscience (IGSN), Ruhr University Bochum, Bochum, Germany.

出版信息

Elife. 2020 Apr 7;9:e53552. doi: 10.7554/eLife.53552.

DOI:10.7554/eLife.53552
PMID:32252889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7138610/
Abstract

Controlling gain of cortical activity is essential to modulate weights between internal ongoing communication and external sensory drive. Here, we show that serotonergic input has separable suppressive effects on the gain of ongoing and evoked visual activity. We combined optogenetic stimulation of the dorsal raphe nucleus (DRN) with wide-field calcium imaging, extracellular recordings, and iontophoresis of serotonin (5-HT) receptor antagonists in the mouse visual cortex. 5-HT1A receptors promote divisive suppression of spontaneous activity, while 5-HT2A receptors act divisively on visual response gain and largely account for normalization of population responses over a range of visual contrasts in awake and anesthetized states. Thus, 5-HT input provides balanced but distinct suppressive effects on ongoing and evoked activity components across neuronal populations. Imbalanced 5-HT1A/2A activation, either through receptor-specific drug intake, genetically predisposed irregular 5-HT receptor density, or change in sensory bombardment may enhance internal broadcasts and reduce sensory drive and vice versa.

摘要

控制皮质活动的增益对于调节内部持续通信和外部感觉驱动之间的权重至关重要。在这里,我们表明,血清素能输入对持续和诱发的视觉活动增益具有可分离的抑制作用。我们在小鼠视觉皮层中结合了背侧中缝核(DRN)的光遗传学刺激与宽场钙成像、细胞外记录和 5-羟色胺(5-HT)受体拮抗剂的离子电渗。5-HT1A 受体促进自发性活动的除法抑制,而 5-HT2A 受体对视觉反应增益进行除法抑制,并在清醒和麻醉状态下在一系列视觉对比范围内对群体反应进行归一化。因此,5-HT 输入对整个神经元群体的持续和诱发活动成分提供了平衡但不同的抑制作用。通过受体特异性药物摄入、遗传倾向的不规则 5-HT 受体密度或感觉轰炸的变化,5-HT1A/2A 的激活不平衡可能会增强内部广播并减少感觉驱动,反之亦然。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/50e806ec281b/elife-53552-fig9-figsupp2.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/5d4978431988/elife-53552-fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/780650914b97/elife-53552-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/f5df00d727ad/elife-53552-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/b50e2215d977/elife-53552-fig8-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/652d/7138610/c81286f0df52/elife-53552-fig8-figsupp2.jpg
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