한빛사논문
Vinod Menon1,2,3,7, Domenic Cerri4,5,6,7, Byeongwook Lee1,7, Rui Yuan1, Sung-Ho Lee4,5,6 & Yen-Yu Ian Shih4,5,6
1Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
2Department of Neurology & Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
3Wu Tsai Neuroscience Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
4Center for Animal MRI, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
5Biomedical Research Imaging Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
6Department of Neurology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
7These authors contributed equally: Vinod Menon, Domenic Cerri, Byeongwook Lee.
Corresponding authors : Correspondence to Vinod Menon or Yen-Yu Ian Shih.
Abstract
The salience network (SN) and default mode network (DMN) play a crucial role in cognitive function. The SN, anchored in the anterior insular cortex (AI), has been hypothesized to modulate DMN activity during stimulus-driven cognition. However, the causal neural mechanisms underlying changes in DMN activity and its functional connectivity with the SN are poorly understood. Here we combine feedforward optogenetic stimulation with fMRI and computational modeling to dissect the causal role of AI neurons in dynamic functional interactions between SN and DMN nodes in the male rat brain. Optogenetic stimulation of Chronos-expressing AI neurons suppressed DMN activity, and decreased AI-DMN and intra-DMN functional connectivity. Our findings demonstrate that feedforward optogenetic stimulation of AI neurons induces dynamic suppression and decoupling of the DMN and elucidates previously unknown features of rodent brain network organization. Our study advances foundational knowledge of causal mechanisms underlying dynamic cross-network interactions and brain network switching.
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