Early-life stress can lead to sustained alterations in regional resting-state brain functions, but the underlying molecular mechanism remains unclear. Stress can also induce sustained changes in epigenetic modificatio...Early-life stress can lead to sustained alterations in regional resting-state brain functions, but the underlying molecular mechanism remains unclear. Stress can also induce sustained changes in epigenetic modifications across brain regions, which are not limited to a few genes;rather, they often tend to produce global levels of change. The functional implication of these changes also remains to be elucidated. We hypothesize that global epigenetic changes may partly modulate the resting-state functions of brain regions to influence behavior. To test this hypothesis, we used an adolescent social stress (ASS) model in mice and examined the relationship between epigenetic modifications and regional resting-state brain activity using resting-state functional magnetic resonance imaging (rs-fMRI). The results showed that, compared to the control mice, the stressed mice showed increased anxiety and social avoidance behaviors and greater levels of dimethylation of histone H3 at lysine 9 (H3K9me2) in the medial prefrontal cortex (mPFC). In addition, the resting-state activity represented by the amplitude of low-frequency fluctuation (ALFF) was significantly lower in the mPFC of stressed mice. To verify the relationship of H3K9me2 and ALFF, the specific inhibition of H3Kme2 was performed by using the drug UNC0642, which reversed the anxiety behavior induced by ASS and significantly increase the ALFF value of mPFC in both normal and ASS animals. Our study is the first to report an association between histone modifications and rs-fMRI findings, providing a new perspective for understanding of the significance of regional brain epigenetic changes and a possible molecular explanation for rs-fMRI findings.展开更多
为了提升轴向磁场磁通切换永磁电机无传感器驱动系统的容错运行性能,本文在6/14极AFFSPMM的基础上提出了一种基于双矢量合成模型预测磁链控制(Two-Vector-Synthesis Model Predictive Flux Control,TVS-MPFC)的容错控制方法。首先,详细...为了提升轴向磁场磁通切换永磁电机无传感器驱动系统的容错运行性能,本文在6/14极AFFSPMM的基础上提出了一种基于双矢量合成模型预测磁链控制(Two-Vector-Synthesis Model Predictive Flux Control,TVS-MPFC)的容错控制方法。首先,详细介绍了TVS-MPFC原理,它在单个工作周期内作用两个电压矢量,并根据磁链矢量跟踪误差最小化原理确定占空比,从而提升控制系统的动稳态性能。然后,在此基础上提出了一种基铜耗最小的转矩分配容错控制方法,并与恒定磁动势容错控制方法进行对比。最后通过实验验证了该容错控制方法的有效性。实验结果表明,所提出的容错控制方法可在电机故障后有效提升AFFSPMM的带载能力,降低电机铜耗,提高AFFSPMM无位置传感器控制系统的容错性能。展开更多
Post-traumatic stress disorder(PTSD)is a severe neuropsychiatric disorder characterised by reexperiencing,avoidance and hyperarousal.Memory abnormalities manifested as intrusive thoughts and prolonged distressful emot...Post-traumatic stress disorder(PTSD)is a severe neuropsychiatric disorder characterised by reexperiencing,avoidance and hyperarousal.Memory abnormalities manifested as intrusive thoughts and prolonged distressful emotions are postulated as key roles in PTSD development and persistence.Over the past decades,convergent results from human and animal studies have systematically investigated contributions of the amygdala,hippocampus and medial prefrontal cortex(mPFC)in fear memory processes,including fear acquisition,storage,reconsolidation and extinction.These findings provide mechanistic insights for cognitive-behavioural therapy and aid in developing pathological region-targeted neuromodulation treatment for PTSD.Taking advantage of advances in cell-type selective labelling and manipulation technologies,recent studies have focused on the spatiotemporal regulation of neural circuits underlying distinct phases of fear memory processes.These findings have revealed that multiple distributed brain areas participate in the fear memory encoding network.Moreover,the functional role of distinct neuronal ensembles within the amygdala-hippocampus-mPFC pathway,identified by genetic markers and projection profiles,has been assigned to temporally separate features of fear processing,demonstrating the sophistication of the fear encoding circuit.These results provide mechanistic insights into PTSD pathology and might shed light on aetiology-based clinical interventions for PTSD.Therefore,the present review will mainly focus on the recent progress in elucidating neural circuit mechanisms underlying the dynamic regulation of fear memory,with an emphasis on the spatial distribution of fear memory encoding neural networks and the temporal coherence between neuronal ensemble activity and fear expression.展开更多
基金the National Natural Science Foundation of China(Grant Nos.82071517,U21A20364,31771217,and 31900731)National Key R&D Program of China(Grant No.2017YFE0126500),and the Scientific Foundation of Institute of Psychology,Chinese Academy of Sciences(No.E2CX4115CX).
文摘Early-life stress can lead to sustained alterations in regional resting-state brain functions, but the underlying molecular mechanism remains unclear. Stress can also induce sustained changes in epigenetic modifications across brain regions, which are not limited to a few genes;rather, they often tend to produce global levels of change. The functional implication of these changes also remains to be elucidated. We hypothesize that global epigenetic changes may partly modulate the resting-state functions of brain regions to influence behavior. To test this hypothesis, we used an adolescent social stress (ASS) model in mice and examined the relationship between epigenetic modifications and regional resting-state brain activity using resting-state functional magnetic resonance imaging (rs-fMRI). The results showed that, compared to the control mice, the stressed mice showed increased anxiety and social avoidance behaviors and greater levels of dimethylation of histone H3 at lysine 9 (H3K9me2) in the medial prefrontal cortex (mPFC). In addition, the resting-state activity represented by the amplitude of low-frequency fluctuation (ALFF) was significantly lower in the mPFC of stressed mice. To verify the relationship of H3K9me2 and ALFF, the specific inhibition of H3Kme2 was performed by using the drug UNC0642, which reversed the anxiety behavior induced by ASS and significantly increase the ALFF value of mPFC in both normal and ASS animals. Our study is the first to report an association between histone modifications and rs-fMRI findings, providing a new perspective for understanding of the significance of regional brain epigenetic changes and a possible molecular explanation for rs-fMRI findings.
文摘为了提升轴向磁场磁通切换永磁电机无传感器驱动系统的容错运行性能,本文在6/14极AFFSPMM的基础上提出了一种基于双矢量合成模型预测磁链控制(Two-Vector-Synthesis Model Predictive Flux Control,TVS-MPFC)的容错控制方法。首先,详细介绍了TVS-MPFC原理,它在单个工作周期内作用两个电压矢量,并根据磁链矢量跟踪误差最小化原理确定占空比,从而提升控制系统的动稳态性能。然后,在此基础上提出了一种基铜耗最小的转矩分配容错控制方法,并与恒定磁动势容错控制方法进行对比。最后通过实验验证了该容错控制方法的有效性。实验结果表明,所提出的容错控制方法可在电机故障后有效提升AFFSPMM的带载能力,降低电机铜耗,提高AFFSPMM无位置传感器控制系统的容错性能。
基金supported by the National Natural Science Foundation of China(82401772)the Shanghai Municipal Education Commission(2021-01-07-00-02-E0086).
文摘Post-traumatic stress disorder(PTSD)is a severe neuropsychiatric disorder characterised by reexperiencing,avoidance and hyperarousal.Memory abnormalities manifested as intrusive thoughts and prolonged distressful emotions are postulated as key roles in PTSD development and persistence.Over the past decades,convergent results from human and animal studies have systematically investigated contributions of the amygdala,hippocampus and medial prefrontal cortex(mPFC)in fear memory processes,including fear acquisition,storage,reconsolidation and extinction.These findings provide mechanistic insights for cognitive-behavioural therapy and aid in developing pathological region-targeted neuromodulation treatment for PTSD.Taking advantage of advances in cell-type selective labelling and manipulation technologies,recent studies have focused on the spatiotemporal regulation of neural circuits underlying distinct phases of fear memory processes.These findings have revealed that multiple distributed brain areas participate in the fear memory encoding network.Moreover,the functional role of distinct neuronal ensembles within the amygdala-hippocampus-mPFC pathway,identified by genetic markers and projection profiles,has been assigned to temporally separate features of fear processing,demonstrating the sophistication of the fear encoding circuit.These results provide mechanistic insights into PTSD pathology and might shed light on aetiology-based clinical interventions for PTSD.Therefore,the present review will mainly focus on the recent progress in elucidating neural circuit mechanisms underlying the dynamic regulation of fear memory,with an emphasis on the spatial distribution of fear memory encoding neural networks and the temporal coherence between neuronal ensemble activity and fear expression.
