Acute stress alters the ‘default’ brain processing (original) (raw)
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Stress Impact on Resting State Brain Networks
PLoS ONE, 2013
Resting state brain networks (RSNs) are spatially distributed large-scale networks, evidenced by resting state functional magnetic resonance imaging (fMRI) studies. Importantly, RSNs are implicated in several relevant brain functions and present abnormal functional patterns in many neuropsychiatric disorders, for which stress exposure is an established risk factor. Yet, so far, little is known about the effect of stress in the architecture of RSNs, both in resting state conditions or during shift to task performance. Herein we assessed the architecture of the RSNs using functional magnetic resonance imaging (fMRI) in a cohort of participants exposed to prolonged stress (participants that had just finished their long period of preparation for the medical residence selection exam), and respective gender-and age-matched controls (medical students under normal academic activities). Analysis focused on the pattern of activity in resting state conditions and after deactivation. A volumetric estimation of the RSNs was also performed. Data shows that stressed participants displayed greater activation of the default mode (DMN), dorsal attention (DAN), ventral attention (VAN), sensorimotor (SMN), and primary visual (VN) networks than controls. Importantly, stressed participants also evidenced impairments in the deactivation of resting statenetworks when compared to controls. These functional changes are paralleled by a constriction of the DMN that is in line with the pattern of brain atrophy observed after stress exposure. These results reveal that stress impacts on activationdeactivation pattern of RSNs, a finding that may underlie stress-induced changes in several dimensions of brain activity.
A large-scale perspective on stress-induced alterations in resting-state networks
Scientific Reports, 2016
Stress is known to induce large-scale neural modulations. However, its neural effect once the stressor is removed and how it relates to subjective experience are not fully understood. Here we used a statistically sound data-driven approach to investigate alterations in large-scale resting-state functional connectivity (rsFC) induced by acute social stress. We compared rsfMRI profiles of 57 healthy male subjects before and after stress induction. Using a parcellation-based univariate statistical analysis, we identified a large-scale rsFC change, involving 490 parcel-pairs. Aiming to characterize this change, we employed statistical enrichment analysis, identifying anatomic structures that were significantly interconnected by these pairs. This analysis revealed strengthening of thalamo-cortical connectivity and weakening of cross-hemispheral parieto-temporal connectivity. These alterations were further found to be associated with change in subjective stress reports. Integrating report-based information on stress sustainment 20 minutes post induction, revealed a single significant rsFC change between the right amygdala and the precuneus, which inversely correlated with the level of subjective recovery. Our study demonstrates the value of enrichment analysis for exploring large-scale network reorganization patterns, and provides new insight on stress-induced neural modulations and their relation to subjective experience. Acute stress has been shown to have dramatic effects on the way our brain functions, which can be viewed as a strategic resource reallocation to functions that are required when facing a threat such as promoting arousal 1,2 and memory encoding of stressful experiences 3-5 , at the cost of higher cognitive functions 6-8. However, while the neural basis of the stress response at the time of induction has been widely investigated, less is known about the neural processes that underlie successive recovery in humans. Characterizing individual variability in recovery from stress is of a particular interest since it has been associated with several stress-related psychopathologies, including Post Traumatic Stress Disorder (PTSD) and depression 9,10. One approach to study post-processing of prior events, such as stress, is by inspecting the spontaneous neural activity that takes place during rest after the event occurred. It has been suggested that this post-processing supports prior experience consolidation 11-13 , and thus, may play a central role in regaining mental and physiological homeostasis, and is expected to involve large scale brain network reorganization 14-16. Accordingly, using post-stress resting-state functional magnetic resonance imaging (rsfMRI) to investigate network reorganization following stress may provide a vital insight into the large-scale neural mechanism that underlies affective recovery from acute stress. Few previous fMRI studies investigated changes in resting-state functional connectivity (rsFC) following acute stress 17-19. For example, van Marle et al. reported increased amygdala rsFC immediately following acute stress with anterior cingulate cortex, anterior insula, and a dorso-rostral pontine region 18. In another study Veer et al. reported increased amygdala rsFC with the posterior cingulate cortex (PCC), precuneus and medial prefrontal cortex an hour following stress, suggesting that these effects could be related to top-down control of the amygdala and consolidation of self-relevant information following a stressful event 19. Lastly, Vaisvaser et al. 17 examined changes in rsFC patterns seeded at the PCC and hippocampus. Unlike the two aforementioned studies, here rsFC
Plasticity of resting state brain networks in recovery from stress
Frontiers in human neuroscience, 2013
Chronic stress has been widely reported to have deleterious impact in multiple biological systems. Specifically, structural and functional remodeling of several brain regions following prolonged stress exposure have been described; importantly, some of these changes are eventually reversible. Recently, we showed the impact of stress on resting state networks (RSNs), but nothing is known about the plasticity of RSNs after recovery from stress. Herein, we examined the "plasticity" of RSNs, both at functional and structural levels, by comparing the same individuals before and after recovery from the exposure to chronic stress; results were also contrasted with a control group. Here we show that the stressed individuals after recovery displayed a decreased resting functional connectivity in the default mode network (DMN), ventral attention network (VAN), and sensorimotor network (SMN) when compared to themselves immediately after stress; however, this functional plastic recove...
Dynamic adaptation of large-scale brain networks in response to acute stressors
Trends in Neurosciences, 2014
Stress initiates an intricate response that affects diverse cognitive and affective domains, with the goal to improve survival chances in the light of changing environmental challenges. Here, we bridge animal data at cellular and systems levels with human work on brain-wide networks to propose a framework describing how stress-related neuromodulators trigger dynamic shifts in network balance, enabling an organism to comprehensively reallocate its neural resources according to cognitive demands. We argue that exposure to acute stress prompts a reallocation of resources to a salience network, promoting fear and vigilance, at the cost of an executive control network. After stress subsides, resource allocation to these two networks reverses, which normalizes emotional reactivity and enhances higher-order cognitive processes important for long-term survival. Hermans et al.-Network adaptation to stress-Page 3 Stress-induced shifts in neurocognition Stress is a double-edged sword: it causes us to have difficulty focusing our attention, retrieving information from memory, and making decisions that require complex thought. Extreme and prolonged stress can furthermore have pathological sequelae such as post-traumatic stress disorder and depression. Yet, the acute stress response also enables us to rapidly detect threats, respond adequately, restore homeostasis when threats are no longer present, and better prepare the organism for future challenges [1,2]. Stressors (see Glossary and Box 1) trigger a chain of neuroendocrine reactions throughout the body that is highly preserved across species [3,4]. Animal work at the cellular level has detailed how stresssensitive neurotransmitters and hormones such as catecholamines and corticosteroids exert modulatory effects on neural excitability and plasticity that are targeted both in space and time [3,5,6]. Spatial specificity allows for selective alterations in widespread target tissues, while temporal specificity allows for timedependent shifts in these changes. At the systems level, stress-related neuromodulators may therefore trigger coordinated, brain-wide shifts in neural functioning that enable us to reallocate processing resources (Box 2) to meet unstable environmental demands [2,7-9]. Here, we integrate animal data at the cellular and systems levels with an emerging human literature on changes in large-scale network properties that subserve adaptive shifts in cognition and behavior [10,11]. We focus our discussion on two such large-scale networks: the salience processing network and the executive control network [12,13]. After summarizing empirical evidence, we propose a model (Fig. 1) that describes how these two networks are regulated in a biphasic and reciprocal fashion in response to acute stressors. Spatially and temporally specific effects of stress-related neuromodulators at the cellular level Animal work has indicated that acute stressors trigger multiple waves of neurochemical changes (Fig. 1A). The earliest responses to acute stressors are mediated by neuropeptides, such as corticotropin-releasing factor, and by catecholamines, such as norepinephrine and dopamine [3]. These changes initiate almost instantly and normalize within 30-60 min. Stress also triggers activation of the hypothalamic-pituitaryadrenal axis, which leads to a surge of corticosteroid production in the adrenal cortex. Peak concentrations in the brain are not reached within 20 minutes after stressor onset [14], which implies that the role of corticosteroids in the immediate stress response must be limited. As we will detail below, these multiple waves of neuromodulatory changes and their interactions allow for intricately timed modulation of distinct neural circuits. Rapid effects of catecholaminergic activation Acute stress promptly activates the locus coeruleus (LC), the brain's primary source of norepinephrine [15,16]. Neurocomputational studies in monkeys show that this leads to a shift from a phasic towards a tonic mode of LC activity, which is associated with enhanced scanning of the environment for potentially salient information [15,17]. Central catecholaminergic activation is followed by activation of the peripheral sympatho-adrenomedullary system, which triggers release of epinephrine from the adrenal medulla. Hermans et al.-Network adaptation to stress-Page 4 Epinephrine further increases norepinephrine release through ascending vagal projections to the nucleus of the solitary tract (NTS) [9]. Noradrenergic projections are widespread and include the entire cerebral cortex, hypothalamus, thalamus, and amygdala [18]. Effects of stress levels of norepinephrine may be regionally specific due to local differences in receptor distribution. While α2A-adrenoceptors in the prefrontal cortex
Exposure to sustained stress can have a profound impact on the brain, emotion and cognition, with either adaptive or maladaptive effects. Human functional brain networks are dynamically organized to enable rapid and flexible adaptation to meet ever-changing task demands. Yet, little is known about how long-term stress alters the dynamic reconfiguration of functional brain networks across multi-task demands. Here we show prominent changes in the dynamic reconfiguration of large-scale brain networks during resting-state, emotional and working-memory processing under long-term stress. Hidden Markov Model analysis detected several latent brain states and switching processes involving the default mode, emotional salience and executive-control networks that are dominant to rest, emotion and working memory, respectively. Critically, long-term stress increased persistent time on brain states relevant to goal-directed demands and cognitive control, with more frequent transitions to these bra...
Stress-induced changes in modular organizations of human brain functional networks
Neurobiology of Stress, 2020
Humans inevitably go through various stressful events, which initiates a chain of neuroendocrine reactions that may affect brain functions and lead to psychopathological symptoms. Previous studies have shown stress-induced changes in activation of individual brain regions or pairwise interregional connectivity. However, it remains unclear how large-scale brain network is reconfigured in response to stress. Using a within-subjects design, we combined the Trier Social Stress Test and graph theoretical method to characterize stress-induced topological alterations of brain functional network. Modularity analysis revealed that the brain network can be divided into frontoparietal, default mode, occipital, subcortical, and central-opercular modules under control and stress conditions, corresponding to several well-known functional systems underpinning cognitive control, self-referential mental processing, visual, salience processing, sensory and motor functions. While the frontoparietal module functioned as a connector module under stress, its within-module connectivity was weakened. The default mode module lost its connector function and its within-module connectivity was enhanced under stress. Moreover, stress altered the capacity to control over information flow in a few regions important for salience processing and self-referential metal processing. Furthermore, there was a trend of negative correlation between modularity and stress response magnitude. These findings demonstrate that acute stress prompts largescale brain-wide reconfiguration involving multiple functional modules.
European Journal of Neuroscience, 2021
Abundant evidence shows that early-life stress (ELS) predisposes for the development of stress-related psychopathology when exposed to stressors later in life, but the underlying mechanisms remain unclear. To study predisposing effects of mild ELS on stress sensitivity, we examined in a healthy human population the impact of a history of ELS on acute stress-related changes in corticolimbic circuits involved in emotional processing (i.e., amygdala, hippocampus and ventromedial prefrontal cortex [vmPFC]). Healthy young male participants (n = 120) underwent resting-state functional magnetic resonance imaging (fMRI) in two separate sessions (stress induction vs. control). The Childhood Trauma Questionnaire (CTQ) was administered to index selfreported ELS, and stress induction was verified using salivary cortisol, blood pressure, heart rate and subjective affect. Our findings show that self-reported ELS was negatively associated with baseline cortisol, but not with the acute stress-induced cortisol response. Critically, individuals with more self-reported ELS exhibited an exaggerated reduction of functional connectivity in corticolimbic circuits under acute stress. A mediation analysis showed that the association between ELS and stress-induced changes in amygdalahippocampal connectivity became stronger when controlling for basal cortisol. Our findings show, in a healthy sample, that the effects of mild ELS on functioning of corticolimbic circuits only become apparent when exposed to an acute stressor and may be buffered by adaptations in hypothalamic-pituitaryadrenal axis function. Overall, our findings might reveal a potential
Stress-induced alterations in large-scale functional networks of the rodent brain
NeuroImage, 2015
Stress-related psychopathology is associated with altered functioning of large-scale brain networks. Animal research into chronic stress, one of the most prominent environmental risk factors for development of psychopathology, has revealed molecular and cellular mechanisms potentially contributing to human mental disease. However, so far, these studies have not addressed the system-level changes in extended brain networks, thought to critically contribute to mental disorders. We here tested the effects of chronic stress exposure (10 days immobilization) on the structural integrity and functional connectivity patterns in the brain, using high-resolution structural MRI, diffusion kurtosis imaging, and resting-state functional MRI, while confirming the expected changes in neuronal dendritic morphology using Golgi-staining. Stress effectiveness was confirmed by a significantly lower body weight and increased adrenal weight. In line with previous research, stressed animals displayed neuronal dendritic hypertrophy in the amygdala and hypotrophy in the hippocampal and medial prefrontal cortex. Using independent component analysis of resting-state fMRI data, we identified ten functional connectivity networks in the rodent brain. Chronic stress appeared to increase connectivity within the somatosensory, visual, and default mode networks. Moreover, chronic stress exposure was associated with an increased volume and diffusivity of the lateral ventricles, whereas no other volumetric changes were observed. This study shows that chronic stress exposure in rodents induces alterations in functional network connectivity strength which partly resemble those observed in stress-related psychopathology. Moreover, these functional consequences of stress seem to be more prominent than the effects on gross volumetric change, indicating their significance for future research.
Stressful experiences modulate neuro-circuitry function, and the temporal trajectory of these alterations, elapsing from early disturbances to late recovery, heavily influences resilience and vulnerability to stress. Such effects of stress may depend on processes that are engaged during resting-state, through active recollection of past experiences and anticipation of future events, all known to involve the default mode network (DMN). By inducing social stress and acquiring resting-state functional magnetic resonance imaging (fMRI) before stress, immediately following it, and 2 h later, we expanded the time-window for examining the trajectory of the stress response. Throughout the study repeated cortisol samplings and self-reports of stress levels were obtained from 51 healthy young males. Post-stress alterations were investigated by whole brain resting-state functional connectivity (rsFC) of two central hubs of the DMN: the posterior cingulate cortex (PCC) and hippocampus. Results indicate a 'recovery' pattern of DMN connectivity, in which all alterations, ascribed to the intervening stress, returned to pre-stress levels. The only exception to this pattern was a stress-induced rise in amygdala-hippocampal connectivity, which was sustained for as long as 2 h following stress induction. Furthermore, this sustained enhancement of limbic connectivity was inversely correlated to individual stress-induced cortisol responsiveness (AUCi) and characterized only the group lacking such increased cortisol (i.e., non-responders). Our observations provide evidence of a prolonged post-stress response profile, characterized by both the comprehensive balance of most DMN functional connections and the distinct time and cortisol dependent ascent of intra-limbic connectivity. These novel insights into neuro-endocrine relations are another milestone in the ongoing search for individual markers in stress-related psychopathologies.
2021
Acute stress in a long period of time could drastically influence one's behavioral and cognitive performances. Therefore, it is important to control the stressful situation and release it after a stressful event. In this regard, understanding of brain mechanism of the stress release will help to introduce new practical approaches. In this study, we hypothesized that induction and release of stress will change the brain functional connectivity pattern. Therefore, by recruiting 20 healthy-subjects and exposing them to stressful events using the trier social stress paradigm, we aimed to investigate patterns of these changes. In a session consist of 23 minutes of psychological stress induction and 20 minutes of recovery, subjects' stress was scored by visual analogue scale (VAS). In addition, salivary cortisol level and EEG data of the subjects were also recorded. Subsequently, brain functional connectivity (FC) maps were calculated in a frequency-specific manner. Then, the effe...