Regional excitation-inhibition balance predicts default-mode network deactivation via functional connectivity.

Regional excitation-inhibition balance predicts default-mode network deactivation via functional connectivity.
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DOI:
10.1016/j.neuroimage.2018.10.055
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发表时间:
2019-01-15
期刊:
影响因子:
5.7
通讯作者:
Yang Y
Yang Y
中科院分区:
医学1区
文献类型:
--
作者:
Gu H;Hu Y;Chen X;He Y;Yang Y

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默认模式网络(DMN)的失活是神经影像学最可靠的观察结果之一,在发育、衰老和各种神经精神疾病中具有重要意义。然而,DMN失活的神经机制仍然难以捉摸。由于区域神经化学底物和区域间神经相互作用的协调在支持大脑功能方面都是必不可少的,因此定量描述它们如何影响DMN失活可能会为该机制提供新的见解。使用n-back工作记忆任务fMRI和磁共振波谱,我们探讨了任务诱导的失活,区域间功能连接和区域兴奋-抑制平衡(谷氨酸/GABA比值评估)在后扣带皮层/楔前叶(PCC/PCU)之间的成对关系。任务诱导的PCC/PCu失活与其兴奋-抑制平衡和区域间功能连接相关,其中具有较低谷氨酸/GABA比率、较强DMN内连接和较强拮抗性DMN间相互作用的参与者具有更大的PCC/PCu失活。中介分析表明,DMN-显着性网络功能的相互作用部分介导的任务引起的失活和兴奋-抑制之间的关系在PCC/PCu。在本研究中发现的三重关系有可能桥接DMN失活相关的研究结果从各种神经影像学方式,并可能提供新的见解DMN失活的神经机制。此外,这一发现可能对与DMN功能障碍相关的神经精神疾病具有重要意义,并建议综合应用基于药理学和神经调节的策略来挽救DMN失活缺陷。
Deactivation of the default mode network (DMN) is one of the most reliable observations from neuroimaging and has significant implications in development, aging, and various neuropsychiatric disorders. However, the neural mechanism underlying DMN deactivation remains elusive. As the coordination of regional neurochemical substrates and interregional neural interactions are both essential in support of brain functions, a quantitative description of how they impact DMN deactivation may provide new insights into the mechanism. Using an n-back working memory task fMRI and magnetic resonance spectroscopy, we probed the pairwise relationship between task-induced deactivation, interregional functional connectivity and regional excitation-inhibition balance (evaluated by glutamate/GABA ratio) in the posterior cingulate cortex/precuneus (PCC/PCu). Task-induced PCC/PCu deactivation correlated with its excitation-inhibition balance and interregional functional connectivity, where participants with lower glutamate/GABA ratio, stronger intra-DMN connections and stronger antagonistic inter-DMN interactions had greater PCC/PCu deactivation. Mediation analyses revealed that the DMN-salience network functional interactions partially mediated the relationship between task-induced deactivation and the excitation-inhibition balance at the PCC/PCu. The triple-relationship discovered in the present study has the potential to bridge DMN-deactivation related findings from various neuroimaging modalities and may provide new insights into the neural mechanism of DMN deactivation. Moreover, this finding may have significant implications for neuropsychiatric disorders related to the DMN dysfunction and suggests an integrated application of pharmacological and neuromodulation-based strategies for rescuing DMN deactivation deficits.
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