Eye-Opening Alters the Interaction Between the Salience Network and the Default-Mode Network.
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ABSTRACT:
SUBMITTER: Han J
PROVIDER: S-EPMC7719144 | biostudies-literature | 2020 Dec
REPOSITORIES: biostudies-literature
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Eye-Opening Alters the Interaction Between the Salience Network and the Default-Mode Network.
Han Junrong J Wu Xuehai X Wu Hang H Wang Dong D She Xuan X Xie Musi M Zhang Fang F Zhang Delong D Zhang Xilin X Qin Pengmin P
Neuroscience bulletin 20200717 12
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Project description:Background:Brain investigations identified salience network (SN) comprising the dorsal Anterior Cingulate Cortex (dACC) and the Anterior Insula (AI). Magnetic resonance spectroscopy (MRS) studies revealed the link between the glutamate concentration in the ACC and alterations in attentional scope. Hence, we investigated whether glutamate concentration in the dACC modulates brain response during salience processing. Methods:Twenty-seven healthy subjects (12?, 15?) provided both STEAM MRS at 7T measuring glutamate concentrations in the dACC as well as a functional magnetic resonance imaging (fMRI) task to study the influence on content-related salience processing and expectedness. Salience was modulated for both sexual and non-sexual emotional photos in either expected or unexpected situations. Correlation between MRS and task fMRI was investigated by performing regression analyses controlling for age, gender, and gray matter partial volume. Results/Conclusion:During picture processing, the extent of deactivation in the Posterior Cingulate Cortex (PCC) was attenuated by two different salience attributions: sexual content and unexpectedness of emotional content. Our results indicate that stimulus inherent salience induces an attenuation of the deactivation in PCC, which is in turn balanced by higher level of glutamate in the dACC.
| S-EPMC6783560 | biostudies-literature
Project description:Schizophrenia and autism spectrum disorder (ASD) are two prevalent neurodevelopmental disorders sharing some similar genetic basis and clinical features. The extent to which they share common neural substrates remains unclear. Resting-state fMRI data were collected from 35 drug-naïve adolescent participants with first-episode schizophrenia (15.6 ± 1.8 years old) and 31 healthy controls (15.4 ± 1.6 years old). Data from 22 participants with ASD (13.1 ± 3.1 years old) and 21 healthy controls (12.9 ± 2.9 years old) were downloaded from the Autism Brain Imaging Data Exchange. Resting-state functional networks were constructed using predefined regions of interest. Multivariate pattern analysis combined with multi-task regression feature selection methods were conducted in two datasets separately. Classification between individuals with disorders and controls was achieved with high accuracy (schizophrenia dataset: accuracy = 83%; ASD dataset: accuracy = 80%). Shared atypical brain connections contributing to classification were mostly present in the default mode network (DMN) and salience network (SN). These functional connections were further related to severity of social deficits in ASD (p = 0.002). Distinct atypical connections were also more related to the DMN and SN, but showed different atypical connectivity patterns between the two disorders. These results suggest some common neural mechanisms contributing to schizophrenia and ASD, and may aid in understanding the pathology of these two neurodevelopmental disorders. Autism Res 2017, 10: 1776-1786. © 2017 International Society for Autism Research, Wiley Periodicals, Inc.Lay summaryAutism spectrum disorder (ASD) and schizophrenia are two common neurodevelopmental disorders which share several genetic and behavioral features. The present study identified common neural mechanisms contributing to ASD and schizophrenia using resting-state functional MRI data. The results may help to understand the pathology of these two neurodevelopmental disorders.
| S-EPMC5685899 | biostudies-literature
Project description:Large-scale brain networks are integral to the coordination of human behaviour, and their anatomy provides insights into the clinical presentation and progression of neurodegenerative illnesses such as Alzheimer's disease, which targets the default mode network, and behavioural variant frontotemporal dementia, which targets a more anterior salience network. Although the default mode network is recruited when healthy subjects deliberate about 'personal' moral dilemmas, patients with Alzheimer's disease give normal responses to these dilemmas whereas patients with behavioural variant frontotemporal dementia give abnormal responses to these dilemmas. We hypothesized that this apparent discrepancy between activation- and patient-based studies of moral reasoning might reflect a modulatory role for the salience network in regulating default mode network activation. Using functional magnetic resonance imaging to characterize network activity of patients with behavioural variant frontotemporal dementia and healthy control subjects, we present four converging lines of evidence supporting a causal influence from the salience network to the default mode network during moral reasoning. First, as previously reported, the default mode network is recruited when healthy subjects deliberate about 'personal' moral dilemmas, but patients with behavioural variant frontotemporal dementia producing atrophy in the salience network give abnormally utilitarian responses to these dilemmas. Second, patients with behavioural variant frontotemporal dementia have reduced recruitment of the default mode network compared with healthy control subjects when deliberating about these dilemmas. Third, a Granger causality analysis of functional neuroimaging data from healthy control subjects demonstrates directed functional connectivity from nodes of the salience network to nodes of the default mode network during moral reasoning. Fourth, this Granger causal influence is diminished in patients with behavioural variant frontotemporal dementia. These findings are consistent with a broader model in which the salience network modulates the activity of other large-scale networks, and suggest a revision to a previously proposed 'dual-process' account of moral reasoning. These findings also characterize network interactions underlying abnormal moral reasoning in frontotemporal dementia, which may serve as a model for the aberrant judgement and interpersonal behaviour observed in this disease and in other disorders of social function. More broadly, these findings link recent work on the dynamic interrelationships between large-scale brain networks to observable impairments in dementia syndromes, which may shed light on how diseases that target one network also alter the function of interrelated networks.
| S-EPMC3673466 | biostudies-literature
Project description:Efficient behavior involves the coordinated activity of large-scale brain networks, but the way in which these networks interact is uncertain. One theory is that the salience network (SN)--which includes the anterior cingulate cortex, presupplementary motor area, and anterior insulae--regulates dynamic changes in other networks. If this is the case, then damage to the structural connectivity of the SN should disrupt the regulation of associated networks. To investigate this hypothesis, we studied a group of 57 patients with cognitive impairments following traumatic brain injury (TBI) and 25 control subjects using the stop-signal task. The pattern of brain activity associated with stop-signal task performance was studied by using functional MRI, and the structural integrity of network connections was quantified by using diffusion tensor imaging. Efficient inhibitory control was associated with rapid deactivation within parts of the default mode network (DMN), including the precuneus and posterior cingulate cortex. TBI patients showed a failure of DMN deactivation, which was associated with an impairment of inhibitory control. TBI frequently results in traumatic axonal injury, which can disconnect brain networks by damaging white matter tracts. The abnormality of DMN function was specifically predicted by the amount of white matter damage in the SN tract connecting the right anterior insulae to the presupplementary motor area and dorsal anterior cingulate cortex. The results provide evidence that structural integrity of the SN is necessary for the efficient regulation of activity in the DMN, and that a failure of this regulation leads to inefficient cognitive control.
| S-EPMC3311356 | biostudies-literature
Project description:Recent research has begun to identify the neural mechanisms underlying the beneficial impact of mindfulness meditation training (MMT) on health and cognition. However, little is known about the effects of MMT on the global interplay of large-scale networks (LSNs) in the brain. In the present study, healthy, meditation-naïve adults (N = 46) underwent resting state fMRI prior to and upon completing 31 days of MMT or an active control intervention. Independent component analysis, sliding time window, and seed-based correlation analyses were performed to assess training-related changes in functional connectivity (FC) within and between networks with relevance to mindfulness meditation. Across sliding time window analyses and seed-based correlation analyses, we found increased FC between nodes of the default mode network (DMN) and nodes of the salience network (SN) in participants of the MMT. Seed-based correlation analyses revealed further connectivity increases between the SN and key regions of the central executive network (CEN). These results indicate, that, among multiple LSNs, one month of mindfulness meditation effectively increases interconnectivity between networks of the triple network model (DMN, SN, CEN), hereby introducing a potential mechanistic concept underlying the beneficial impact of MMT.Clinical trial registration: This study is listed as a clinical trial on the ISRCTN registry with trial ID ISRCTN95197731 (date of first registration: 15/02/2022).
| S-EPMC9346127 | biostudies-literature
Project description:Default mode network (DMN) is a functional brain network with a unique neural activity pattern that shows high activity in resting states but low activity in task states. This unique pattern has been proved to relate with higher cognitions such as learning, memory and decision-making. But neural mechanisms of interactions between the default network and the task-related network are still poorly understood. In this paper, a theoretical model of coupling the DMN and working memory network (WMN) is proposed. The WMN and DMN both consist of excitatory and inhibitory neurons connected by AMPA, NMDA, GABA synapses, and are coupled with each other only by excitatory synapses. This model is implemented to demonstrate dynamical processes in a working memory task containing encoding, maintenance and retrieval phases. Simulated results have shown that: (1) AMPA channels could produce significant synchronous oscillations in population neurons, which is beneficial to change oscillation patterns in the WMN and DMN. (2) Different NMDA conductance between the networks could generate multiple neural activity modes in the whole network, which may be an important mechanism to switch states of the networks between three different phases of working memory. (3) The number of sequentially memorized stimuli was related to the energy consumption determined by the network's internal parameters, and the DMN contributed to a more stable working memory process. (4) Finally, this model demonstrated that, in three phases of working memory, different memory phases corresponded to different functional connections between the DMN and WMN. Coupling strengths that measured these functional connections differed in terms of phase synchronization. Phase synchronization characteristics of the contained energy were consistent with the observations of negative and positive correlations between the WMN and DMN reported in referenced fMRI experiments. The results suggested that the coupled interaction between the WMN and DMN played important roles in working memory.Supplementary informationThe online version contains supplementary material available at 10.1007/s11571-021-09674-1.
| S-EPMC8572310 | biostudies-literature
Project description:While chronic cocaine use is associated with abnormalities in both brain structure and function within and interactions between regions, previous studies have been limited to interrogating structure and function independently, and the detected neural differences have not been applied to independent samples to assess the clinical relevance of results. We investigated consequences of structural differences on resting-state functional connectivity in cocaine addiction and tested whether resting-state functional connectivity of the identified circuits predict relapse in an independent cohort. Subjects included 64 non-treatment-seeking cocaine users (NTSCUs) and 67 healthy control subjects and an independent treatment-completed cohort (n = 45) of cocaine-dependent individuals scanned at the end of a 30-day residential treatment programme. Differences in cortical thickness and related resting-state functional connectivity between NTSCUs and healthy control subjects were identified. Survival analysis, applying cortical thickness of the identified regions, resting-state functional connectivity of the identified circuits and clinical characteristics to the treatment cohort, was used to predict relapse. Lower cortical thickness in bilateral insula and higher thickness in bilateral temporal pole were found in NTSCUs versus healthy control subjects. Whole brain resting-state functional connectivity analyses with these four different anatomical regions as seeds revealed eight weaker circuits including within the salience network (insula seeds) and between temporal pole and elements of the default mode network in NTSCUs. Applying these circuits and clinical characteristics to the independent cocaine-dependent treatment cohort, functional connectivity between right temporal pole and medial prefrontal cortex, combined with years of education, predicted relapse status at 150 days with 88% accuracy. Deficits in the salience network suggest an impaired ability to process physiologically salient events, while abnormalities in a temporal pole-medial prefrontal cortex circuit might speak to the social-emotional functional alterations in cocaine addiction. The involvement of the temporal pole-medial prefrontal cortex circuit in a model highly predictive of relapse highlights the importance of social-emotional functions in cocaine dependence, and provides a potential underlying neural target for therapeutic interventions, and for identifying those at high risk of relapse.
| S-EPMC6075550 | biostudies-other
Project description:BackgroundRecent functional imaging studies on chronic pain of various organic etiologies have shown significant alterations in both the spatial and the temporal dimensions of the functional connectivity of the human brain in its resting state. However, it remains unclear whether similar changes in intrinsic connectivity networks (ICNs) also occur in patients with chronic pain disorder, defined as persistent, medically unexplained pain.MethodsWe compared 21 patients who suffered from chronic pain disorder with 19 age- and gender-matched controls using 3T-fMRI. All neuroimaging data were analyzed using both independent component analysis (ICA) and power spectra analysis.ResultsIn patients suffering from chronic pain disorder, the fronto-insular 'salience' network (FIN) and the anterior default mode network (aDMN) predominantly oscillated at higher frequencies (0.20 - 0.24 Hz), whereas no significant differences were observed in the posterior DMN (pDMN) and the sensorimotor network (SMN).ConclusionsOur results indicate that chronic pain disorder may be a self-sustaining and endogenous mental process that affects temporal organization in terms of a frequency shift in the rhythmical dynamics of cortical networks associated with emotional homeostasis and introspection.
| S-EPMC3616999 | biostudies-literature
Project description:Aerobic training (AT) is a promising intervention to improve cognitive functioning. However, its modulatory effects on brain networks are not yet entirely understood. Sixty-five subjects with mild cognitive impairment performed a moderate intensity, 24-week AT program. Differences in resting regional brain glucose metabolism (rBGM) with FDG-PET were assessed before and after AT on a voxel-by-voxel basis. Structural equation modeling was used to create latent variables based on regions with significant rBGM changes and to test a hypothetical model about the inter-relationships between these changes. There were significant rBGM reductions in both anterior temporal lobes (ATL), left inferior frontal gyrus, left anterior cingulate cortex, right hippocampus, left meddle frontal gyrus and bilateral caudate nuclei. In contrast, there was an increase in rBGM in the right precuneus and left inferior frontal gyrus. Latent variables reflecting the salience network and ATL were created, while the precuneus represented the default mode network. In the model, salience network rBGM was decreased after AT. In contrast, rBGM in the default mode network increased as a final outcome. This result suggested improved salience network efficacy and increased control over other brain functional networks. The ATL network decreased its rBGM and connected to the salience network and default mode network with positive and negative correlations, respectively. The model fit values reached statistical significance, demonstrating that this model explained the variance in the measured data. In mild cognitive impairment subjects, AT modulated rBGM in salience network and default mode network nodes. Such changes were in the direction of the normally expected resting-state metabolic patterns of these networks.
| S-EPMC6031093 | biostudies-literature
Project description:IntroductionIn recent years, treatment of intractable epilepsy has become more challenging, due to an increase in resistance to antiepileptic drugs, as well as diminished success following resection surgery. Here, we present the case of a 19-year old epileptic patient who received vagus nerve stimulation (VNS) following unsuccessful left parietal-occipital lesion-resection surgery, with results indicating an approximate 50% reduction in seizure frequency and a much longer seizure-free interictal phase.Materials and methodsUsing resting-state functional magnetic resonance imaging, we measured the changes in resting-state brain networks between pre-VNS treatment and 6 months post-VNS, from the perspective of regional and global variations, using regional homogeneity and large-scale functional connectives (seeding posterior cingulate cortex and anterior cingulate cortex), respectively.ResultsAfter 6 months of VNS therapy, the resting-state brain networks were slightly reorganized in regional homogeneity, mainly in large-scale functional connectivity, where excessive activation of the salience network was suppressed, while at the same time the suppressed default-mode network was activated.ConclusionWith regard to resting-state brain networks, we propose a hypothesis based on this single case study that VNS acts on intractable epilepsy by modulating the balance between salience and default-mode networks through the integral hub of the anterior cingulate cortex.
| S-EPMC5067064 | biostudies-literature