Altered Negative BOLD Responses in the Default-Mode Network during Emotion Processing in Depressed Subjects

Grimm, Simone; Boesiger, Peter; Beck, Johannes; Schuepbach, Daniel; Bermpohl, Felix; Walter, Martin; Ernst, Jutta; Hell, Daniel; Boeker, Heinz; Northoff, Georg

doi:10.1038/npp.2008.81

Cited by 321 publications

(256 citation statements)

References 53 publications

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“…This is of particular interest because resting-state DMN dominance is associated with increased maladaptive, depressive rumination, and reduced adaptive, reflective rumination (32). Depressed patients typically fail to down-regulate DMN activity during emotional stimulation (33,34). Our finding of reduced intrinsic DMN connectivity after sleep deprivation resembles a pattern of normalization with regard to the depressive state.…”

Section: Discussionmentioning

confidence: 60%

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Bosch

Rihm

Scheidegger

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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In many patients with major depressive disorder, sleep deprivation, or wake therapy, induces an immediate but often transient antidepressant response. It is known from brain imaging studies that changes in anterior cingulate and dorsolateral prefrontal cortex activity correlate with a relief of depression symptoms. Recently, resting-state functional magnetic resonance imaging revealed that brain network connectivity via the dorsal nexus (DN), a cortical area in the dorsomedial prefrontal cortex, is dramatically increased in depressed patients. To investigate whether an alteration in DN connectivity could provide a biomarker of therapy response and to determine brain mechanisms of action underlying sleep deprivations antidepressant effects, we examined its influence on resting state default mode network and DN connectivity in healthy humans. Our findings show that sleep deprivation reduced functional connectivity between posterior cingulate cortex and bilateral anterior cingulate cortex (Brodmann area 32), and enhanced connectivity between DN and distinct areas in right dorsolateral prefrontal cortex (Brodmann area 10). These findings are consistent with resolution of dysfunctional brain network connectivity changes observed in depression and suggest changes in prefrontal connectivity with the DN as a brain mechanism of antidepressant therapy action.

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Section: Discussionmentioning

confidence: 60%

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Bosch

Rihm

Scheidegger

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…These CPS findings are of translational interest, given that FCs within and between regions comprising the DMN, namely cingulate, prefrontal, parietal and temporal cortices, are also increased in humans in states of chronic stress or depression (Broyd et al, 2009;Grimm et al, 2009;Soares et al, 2013;Whitfield-Gabrieli and Ford, 2012). Connectivity within the human DMN is proposed to relate to self-absorption and rumination.…”

Section: Increases In Within-and Between-network Functional Connectivmentioning

confidence: 91%

“…For example, the default mode network (DMN), involving cingulate, prefrontal, parietal and temporal cortices (Broyd et al, 2009), is proposed to relate to self-absorption and rumination. In fact, FC within the DMN is increased by stress (Soares et al, 2013) and in depression (Grimm et al, 2009;Whitfield-Gabrieli and Ford, 2012). In addition to these analyses of the changes in brain function underlying depression, region-specific metabolic changes as derived from MRS have been reported for depressed patients (Hasler et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Chronic psychosocial stress in mice leads to changes in brain functional connectivity and metabolite levels comparable to human depression

et al. 2016

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Human depression, for which chronic psychosocial stress is a major risk factor, is characterized by consistent alterations in neurocircuitry. For example, there is increased functional connectivity (FC) within and between regions comprising the default mode network (DMN) including prefrontal cortex and cingulate cortex. Alterations in network FC are associated with specific aspects of psychopathology. In mice, chronic psychosocial stress (CPS) leads to depression-relevant behavior, including increased fear learning, learned helplessness, fatigue and decreased motivation for reward. Using multimodal in vivo magnetic resonance imaging (MRI) and spectroscopy (MRS), we investigated CPS effects on function and structure in the mouse brain under light anesthesia. Mice underwent a baseline MRI/MRS session, followed by 15-day CPS (n=26) or control handling (n=27), and a post-treatment MRI/MRS session. In BOLD fMRI, relative to controls, CPS mice exhibited robust, reproducible increases in FC within 8 of 9 identified cortical networks, including the prefrontal and cingulate cortices that contribute to the "mouse DMN". CPS mice exhibited increases in between-network FC, including amygdala -prefrontal cortex and amygdala -cingulate cortex. MRS identified metabolic alterations in CPS mice as increased inositol levels in amygdala and increased glycerophosphorylcholine levels in prefrontal cortex. Diffusion-weighted MRI detected increased fractional anisotropic values in the cingulum. This study demonstrates that chronic psychosocial stress induces FC states in the mouse brain analogous to those observed in depression, as well as cerebral metabolism and white matter pathway alterations that contribute to understanding of pathological processes. It also demonstrates the importance of brain imaging to the establishment of valid animal models in translational psychiatry. AbstractHuman depression, for which chronic psychosocial stress is a major risk factor, is characterized by consistent alterations in neurocircuitry. For example, there is increased functional connectivity (FC) within and between regions comprising the default mode network (DMN) including prefrontal cortex and cingulate cortex. Alterations in network FC are associated with specific aspects of psychopathology. In mice, chronic psychosocial stress (CPS) leads to depression-relevant behavior, including increased fear learning, learned helplessness, fatigue and decreased motivation for reward.Using multimodal in vivo magnetic resonance imaging (MRI) and spectroscopy (MRS), we investigated CPS effects on function and structure in the mouse brain under light anesthesia. Mice underwent a baseline MRI/MRS session, followed by 15-day CPS (n=26) or control handling (n=27), and a posttreatment MRI/MRS session. In BOLD fMRI, relative to controls, CPS mice exhibited robust, reproducible increases in FC within 8 of 9 identified cortical networks, including the prefrontal and cingulate cortices that contribute to the "mouse DMN". CPS mice exhibited increases in b...

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“…This is called TP-deficiency. Interestingly, both TNpersistence and TP-deficiency have been reported in mental disorders (Grimm et al, 2009;Hooley et al, 2005;Mitterschiffthaler et al, 2008;Sheline et al, 2009) as well as in some conditions in healthy participants (Polli et al, 2005;Weissman et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

et al. 2012

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A neurobiological account of cognitive vulnerability for recurrent depression is presented based on recent developments of resting state neural networks. We propose that alterations in the interplay between task positive (TP) and task negative (TN) elements of the Default Mode Network (DMN) act as a neurobiological risk factor for recurrent depression mediated by cognitive mechanisms. In the framework, depression is characterized by an imbalance between TN-TP components leading to an overpowering of TP by TN activity. The TN-TP imbalance is associated with a dysfunctional internally-focused cognitive style as well as a failure to attenuate TN activity in the transition from rest to task. Thus we propose the TN-TP imbalance as overarching neural mechanism involved in crucial cognitive risk factors for recurrent depression, namely rumination, impaired attentional control, and cognitive reactivity. During remission the TN-TP imbalance persists predisposing to vulnerability of recurrent depression. Empirical data to support this model is reviewed. Finally, we specify how this framework can guide future research efforts.

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Altered Negative BOLD Responses in the Default-Mode Network during Emotion Processing in Depressed Subjects

Cited by 321 publications

References 53 publications

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Chronic psychosocial stress in mice leads to changes in brain functional connectivity and metabolite levels comparable to human depression

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

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