Endogenous cortisol is associated with functional connectivity between the amygdala and medial prefrontal cortex (original) (raw)
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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.
The brain and the stress axis: The neural correlates of cortisol regulation in response to stress
Neuroimage, 2009
The hypothalamic-pituitary-adrenal (HPA) axis is the major endocrine stress axis of the human organism. Cortisol, the final hormone of this axis, affects metabolic, cardiovascular and central nervous systems both acutely and chronically. Recent advances in neuroimaging techniques have led to the investigation of regulatory networks and mechanisms of cortisol regulation in the central nervous system in human populations. In the following review, results from human and animal studies are being presented that investigate the specific role of hippocampus (HC), amygdala (AG), prefrontal cortex (PFC), and brainstem nuclei in cortisol regulation in response to stress. In general, the types of stressors need to be distinguished when discussing the contributions of these structures in regulating the HPA axis. We propose a basic framework on how these structures communicate as a network to regulate cortisol secretion in response to psychological stress. Furthermore, we review critical studies that have substantially contributed to the literature. Possible future research avenues in the field of neuroimaging of cortisol regulation are discussed. In combination with investigations on genetic and environmental factors that influence the development of the HPA axis, this emerging new research will eventually allow the formulation of a more comprehensive framework of functional neuroanatomy of cortisol regulation.
Journal of Neuroendocrinology, 2015
Responding to real or potential threats in the environment requires the coordination of autonomic, neuroendocrine and behavioural processes to promote adaptation and survival. These diverging systems necessitate input from the limbic forebrain to integrate and modulate functional output in accordance with contextual demand. In the present review, we discuss the potential role of the medial prefrontal cortex (mPFC) as a coordinator of behavioural and physiological stress responses across multiple temporal and contextual domains. Furthermore, we highlight converging evidence from rodent and human research indicating the necessity of the mPFC for modulating physiological energetic systems to mobilise or limit energetic resources as needed to ultimately promote behavioural adaptation in the face of stress. We review the literature indicating that glucocorticoids act as one of the primary messengers in the reallocation of energetic resources having profound effects locally within the mPFC, as well as shaping how the mPFC acts within a network of brain structures to modulate responses to stress. Finally, we discuss how both rodent and human studies point toward a critical role of the mPFC in the coordination of anticipatory responses to stress and why this distinction is an important one to make in stress neurobiology.
Can the neural–cortisol association be moderated by experience-induced changes in awareness?
Scientific Reports, 2015
Cortisol homeostasis is important for cognitive and affective functions that depend on cortisolsensitive brain regions including the hippocampus and prefrontal cortex. Recent studies have shown that training induces changes in the brain. We report the findings of a longitudinal study that verified the moderation effect of experience-induced changes in awareness on the neural-cortisol association in cortisol-sensitive brain regions. These findings provide the first piece of evidence that planned behavioral experience can moderate the neural-cortisol association. A range of changes in awareness was achieved in a sample of 21 Chinese participants, divided into two groups: Awarenessbased compassion meditation (ABCM) (n = 10) and relaxation (n = 11). We observed that changes in awareness were significant moderators of hippocampal-cortisol changes. Furthermore, a significant negative association between changes in plasma cortisol level and the resting-state synchrony of the right hippocampal and insular-frontal-operculum regions was observed. These novel findings shed light on the interrelationships between changes in hippocampal-cortisol levels and changes in awareness and preliminarily identify the neural underpinnings of interventions for cortisol-related abnormal functioning for further study. Neuroplasticity underlies changes in neural pathways and synapses of the human neural system, and it plays an important role in the modification of neural communication with the endocrine system to produce adaptive responses to life changes 1,2. In fact, the nervous and endocrine systems contribute to a large proportion of human bodily functions, and these two systems are interrelated via different pathways. One of the well-studied pathways is the hypothalamus-pituitary-adrenal (HPA) axis, which regulates peripheral cortisol levels. Disruption of cortisol homeostasis is associated with various cognitive and affective dysfunctions. For example, elevated plasma cortisol levels are associated with major depressive disorder 3 , and lower plasma cortisol levels may be associated with emotional numbing symptomatology in people with posttraumatic stress disorder 4. Cortisol also plays a role in neuroplasticity. The effect of peripheral cortisol levels on neuroplastic changes involves brain regions that express glucocorticoid receptors, such as the hippocampus 5. A recent study demonstrated that changes in peripheral cortisol levels under stress conditions have important implications on the functioning of neural structures of the default-mode network (DMN), including the hippocampus, which likely actively retrieves past experiences, anticipates future events 6 , and regulates our mind-wandering activity 7. Furthermore, the intake of hydrocortisone may affect resting-state functional coupling of neural substrates that are important
Brain, behavior, and immunity, 2015
Psychological stress is implicated in the etiology of many common chronic diseases and mental health disorders. Recent research suggests that inflammation may be a key biological mediator linking stress and health. Nevertheless, the neurocognitive pathways underlying stress-related increases in inflammatory activity are largely unknown. The present study thus examined associations between neural and inflammatory responses to an acute laboratory-based social stressor. Healthy female participants (n=31) were exposed to a brief episode of stress while they underwent an fMRI scan. Blood samples were taken before and after the stressor, and plasma was assayed for markers of inflammatory activity. Exposure to the stressor was associated with significant increases in feelings of social evaluation and rejection, and with increases in levels of inflammation. Analyses linking the neural and inflammatory data revealed that heightened neural activity in the amygdala in response to the stressor ...
Stress Induction and Release: Electroencephalography Study on Brain Networks and Cortisol
Basic and Clinical Neuroscience Journal, 2024
Acute stress over a long time period can drastically influence the behavioral and cognitive performances. Therefore, it is important to control and eliminate the stressor after a stressful event. In this regard, understanding of brain mechanism of stress release will help to introduce new practical approaches. In this study, we aimed to investigate the changes in the brain's functional connectivity (FC) patterns and salivary cortisol level during stress induction and release in healthy young male adults. Method: In this study, 20 healthy young male adults were exposed to stressful events using the Trier social stress paradigm in one session consisting of 23 minutes of psychological stress induction and 20 minutes of recovery, Their stress was measured by the visual analog scale (VAS). In addition, their salivary cortisol levels and electroencephalography (EEG) data were recorded. Subsequently, brain FC maps were prepared in a frequency-specific manner. Then, the effects of inducing and releasing stress on the VAS, cortisol level, and FC were assessed. Results: The inter-hemispheric FC of the right frontal lobes with other brain regions decreased, while the FC was increased in the left frontal lobes during the induction of stress. Interestingly, the release of stress presented a recovery pattern of inter-hemispheric FC. These changes in FC significantly correlated with changes in the cortisol level. Conclusion: Our findings highlight the important role of bihemispheric associations in adaptation and coping with stressful conditions.
Sex differences in the functional connectivity of the amygdalae in association with cortisol
NeuroImage, 2016
Human amygdalae are involved in various behavioral functions such as affective and stress processing. For these behavioral functions, as well as for psychophysiological arousal including cortisol release, sex differences are reported. Here, we assessed cortisol levels and resting-state functional connectivity (rsFC) of left and right amygdalae in 81 healthy participants (42 women) to investigate potential modulation of amygdala rsFC by sex and cortisol concentration.
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...
European Journal of Neuroscience, 1999
The amygdala plays a pivotal role in the generation of appropriate responses to emotional stimuli. In the case of emotional stressors, these responses include activation of the hypothalamic±pituitary±adrenal (HPA) axis. This effect is generally held to depend upon the central nucleus of the amygdala, but recent evidence suggests a role for the medial nucleus. In the present study, c-fos expression, amygdala lesion and retrograde tracing experiments were performed on adult rats in order to re-evaluate the role of the central as opposed to the medial amygdala in generating neuroendocrine responses to an emotional stressor. Brief restraint (15 min) was used as a representative emotional stressor and was found to elicit c-fos expression much more strongly in the medial than central nucleus of the amygdala; relatively few Fos-positive cells were seen in other amygdala nuclei. Subsequent experiments showed that ibotenic acid lesions of the medial amygdala, but not the central amygdala, greatly reduced restraint-induced activation of cells of the medial paraventricular nucleus, the site of the tuberoinfundibular corticotropin-releasing factor cells that constitute the apex of the HPA axis. Medial amygdala lesions also reduced the activation of supraoptic and paraventricular nucleus oxytocinergic neurosecretory cells that commonly accompanies stress-induced HPA axis activation in rodents. To assess whether the role of the medial amygdala in the control of neuroendocrine cell responses to emotional stress might involve a direct projection to such cells, retrograde tracing of amygdala projections to the paraventricular nucleus was performed in combination with Fos immunolabelling. This showed that although some medial amygdala cells activated by exposure to an emotional stressor project directly to the paraventricular nucleus, the number is very small. These ®ndings provide the ®rst direct evidence that it is the medial rather than the central amygdala that is critical to hypothalamic neuroendocrine cell responses during an emotional response, and also provide the ®rst evidence that the amygdala governs oxytocin as well as HPA axis responses to an emotional stressor.
Journal of …, 2006
Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamicpituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62-to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease Ͻ attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.