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生长抑素神经元调控由显著视觉信号诱导的θ振荡。

Somatostatin Neurons Govern Theta Oscillations Induced by Salient Visual Signals.

机构信息

Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China; MoE Key Laboratory for Biomedical Photonics, Collaborative Innovation Center for Biomedical Engineering, School of Engineering Sciences, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.

Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China; MoE Key Laboratory for Biomedical Photonics, Collaborative Innovation Center for Biomedical Engineering, School of Engineering Sciences, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China.

出版信息

Cell Rep. 2020 Nov 24;33(8):108415. doi: 10.1016/j.celrep.2020.108415.

Abstract

Salient visual stimuli enhance theta oscillations and spike-phase locking in the theta band in the primary visual cortex (V1) of mice; however, the detailed mechanisms remain unknown. GABAergic neurons play a vital role in regulating these oscillations. Here, we use optogenetic recordings to tag cell-type-specific neurons in V1 of head-fixed mice and demonstrate that salient visual stimuli facilitate somatostatin (SOM)-expressing neuron responses and firing with theta band oscillations but suppress activities of parvalbumin (PV)-expressing neurons. Furthermore, inactivation of SOM neurons attenuates the enhancement of theta oscillations induced by salient visual stimuli and rhythmic activation of SOM neurons enhances theta oscillations. These results reveal a potential cortical theta oscillation mechanism governed by SOM neurons.

摘要

显著的视觉刺激增强了小鼠初级视觉皮层 (V1) 中的θ振荡和在θ频段的尖峰相位锁定;然而,详细的机制仍然未知。GABA 能神经元在调节这些振荡中起着至关重要的作用。在这里,我们使用光遗传学记录标记固定头部的小鼠 V1 中的细胞类型特异性神经元,并证明显著的视觉刺激促进了含有生长抑素 (SOM) 的神经元的反应和以θ频段振荡的放电,但抑制了含有钙调蛋白结合蛋白 2 (PV) 的神经元的活动。此外,SOM 神经元的失活减弱了显著的视觉刺激引起的θ振荡的增强,而 SOM 神经元的节律性激活增强了θ振荡。这些结果揭示了一个由 SOM 神经元控制的潜在的皮层θ振荡机制。

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