scholarly journals Structural covariance of amygdala subregions is associated with trait aggression and endogenous testosterone in healthy individuals

2021 ◽  
Author(s):  
Martin Gottlich ◽  
Macia Buades Rotger ◽  
Juliana Wiechert ◽  
Frederike Beyer ◽  
Ulrike M. Kramer

Many studies point toward volume reductions in the amygdala as a potential neurostructural marker for trait aggression. However, most of these findings stem from clinical samples, rendering unclear whether the findings generalize to non-clinical populations. Furthermore, the notion of neural networks suggests that interregional correlations in grey matter volume (i.e., structural covariance) can explain individual differences in aggressive behavior beyond local univariate associations. Here, we tested whether structural covariance between amygdala subregions and the rest of the brain is associated with self-reported aggression in a large sample of healthy young students (n=263; 51% women). Salivary testosterone concentrations were measured for a subset of n=76 participants (45% women), allowing us to investigate the influence of endogenous testosterone on structural covariance. Aggressive individuals showed enhanced covariance between superficial amygdala (SFA) and dorsal anterior insula (dAI), but lower covariance between laterobasal amygdala (LBA) and dorsolateral prefrontal cortex (dlPFC). These structural patterns overlap with functional networks involved in the genesis and regulation of aggressive behavior, respectively. With increasing endogenous testosterone, we observed stronger structural covariance between centromedial amygdala (CMA) and medial prefrontal cortex in men and between CMA and orbitofrontal cortex in women. These results speak for structural covariance of amygdala subregions as a robust correlate of trait aggression in healthy individuals. Moreover, regions that showed structural covariance with the amygdala modulated by either testosterone or aggression did not overlap, speaking for a more complex role of testosterone in human social behavior rather than the simple assumption that testosterone only increases aggressiveness.

2004 ◽  
Vol 29 (10) ◽  
pp. 1918-1924 ◽  
Author(s):  
Paolo Brambilla ◽  
Jeffrey A Stanley ◽  
Roberto B Sassi ◽  
Mark A Nicoletti ◽  
Alan G Mallinger ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Aurélie L. Manuel ◽  
Nicholas W. G. Murray ◽  
Olivier Piguet

AbstractDelay discounting requires computing trade-offs between immediate-small rewards and later-larger rewards. Negative and positive emotions shift decisions towards more or less impulsive responses, respectively. Models have conceptualized this trade-off by describing an interplay between “emotional” and “rational” processes, with the former involved during immediate choices and relying on the ventromedial prefrontal cortex (vmPFC), and the latter involved in long-term choices and relying on the dorsolateral prefrontal cortex (dlPFC). Whether stimulation of the vmPFC modulates emotion-induced delay discounting remains unclear. We applied tDCS over the vmPFC in 20 healthy individuals during a delay discounting task following an emotional (positive, negative) or neutral induction. Our results showed that cathodal tDCS increased impulsivity after positive emotions in high impulsivity trials. For low impulsivity trials, anodal tDCS decreased impulsivity following neutral induction compared with emotional induction. Our findings demonstrate that the vmPFC integrates reward and emotion most prominently in situations of increased impulsivity, whereas when higher cognitive control is required the vmPFC appears to be less engaged, possibly due to recruitment of the dlPFC. Understanding how stimulation and emotion influence decision-making at the behavioural and neural levels holds promise to develop interventions to reduce impulsivity.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Xu ◽  
Yutong Zhang ◽  
Chen Wang ◽  
Huaqiang Liao ◽  
Siyuan Zhou ◽  
...  

Abstract The pathophysiological differences between menstrually-related migraine (MRM) and pure menstrual migraine (PMM) are largely unclear. The aim of this study was to investigate the potential differences in brain structure and function between PMM and MRM. Forty-eight menstrual migraine patients (32 MRM; 16 PMM) were recruited for this study. Voxel-based morphometry (VBM) was applied on structural magnetic resonance imaging (sMRI), and the amplitude of low-frequency fluctuations (ALFF) and regional homogeneity (ReHo) in resting state functional MRI (rsfMRI) were calculated. No significant between-group difference was observed in the grey matter volume (GMV). MRM patients exhibited lower ALFF values at the dorsolateral prefrontal cortex (DLPFC) and medial prefrontal cortex (mPFC) than PMM patients. Moreover, the MRM group showed significantly higher ReHo values in the DLPFC. Higher values in the mPFC were related to higher expression of calcitonin gene-associated peptide (CGRP) in the PMM group (r = 0.5, P = 0.048). Combined ALFF and ReHo analyses revealed significantly different spontaneous neural activity in the DLPFC and mPFC, between MRM and PMM patients, and ALFF values in the mPFC were positively correlated with CGRP expression, in the PMM group. This study enhances our understanding of the relationship between neural abnormalities and CGRP expression in individuals with PMM.


2022 ◽  
Vol 165 ◽  
pp. 108113
Author(s):  
Martin Göttlich ◽  
Macià Buades-Rotger ◽  
Juliana Wiechert ◽  
Frederike Beyer ◽  
Ulrike M. Krämer

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
G. R. Wylie ◽  
B. Yao ◽  
H. M. Genova ◽  
M. H. Chen ◽  
J. DeLuca

AbstractCognitive fatigue, or fatigue related to mental work, is a common experience. A growing body of work using functional neuroimaging has identified several regions that appear to be related to cognitive fatigue and that potentially comprise a “fatigue network”. These include the striatum of the basal ganglia, the dorsolateral prefrontal cortex (DLPFC), the dorsal anterior cingulate cortex (dACC), the ventro-medial prefrontal cortex (vmPFC) and the anterior insula. However, no work has been conducted to assess whether the connectivity between these regions changes as a function of cognitive fatigue. We used a task-based functional neuroimaging paradigm to induce fatigue in 39 healthy individuals, regressed the signal associated with the task out of the data, and investigated how the functional connectivity between these regions changed as cognitive fatigue increased. We observed functional connectivity between these regions and other frontal regions largely decreased as cognitive fatigue increased while connectivity between these seeds and more posterior regions increased. Furthermore the striatum, the DLPFC, the insula and the vmPFC appeared to be central ‘nodes’ or hubs of the fatigue network. These findings represent the first demonstration that the functional connectivity between these areas changes as a function of cognitive fatigue.


2018 ◽  
Vol 2 ◽  
pp. 247054701878639 ◽  
Author(s):  
Sophie E. Holmes ◽  
Dustin Scheinost ◽  
Nicole DellaGioia ◽  
Margaret T. Davis ◽  
David Matuskey ◽  
...  

Background Neuroimaging studies have revealed that disturbances in network organization of key brain regions may underlie cognitive and emotional dysfunction in posttraumatic stress disorder (PTSD). Examining both brain structure and function in the same population may further our understanding of network alterations in PTSD. Methods We used tensor-based morphometry and intrinsic connectivity distribution to identify regions of altered volume and functional connectivity in unmedicated individuals with PTSD ( n = 21) and healthy comparison participants ( n = 18). These regions were then used as seeds for follow-up anatomical covariance and functional connectivity analyses. Results Smaller volume in the cerebellum and weaker structural covariance between the cerebellum seed and the middle temporal gyrus were observed in the PTSD group. Individuals with PTSD also exhibited lower whole-brain connectivity in the cerebellum, dorsolateral prefrontal cortex (dlPFC) and medial prefrontal cortex. Functional connectivity in the cerebellum and grey matter volume in the dlPFC were negatively correlated with PTSD severity as measured by the DSM-5 PTSD Checklist (PCL-5; r = −.0.77, r = − 0.79). Finally, seed connectivity revealed weaker connectivity within nodes of the central executive network (right and left dlPFC), and between nodes of the default mode network (medial prefrontal cortex and cerebellum) and the supramarginal gyrus, in the PTSD group. Conclusion We demonstrate structural and functional alterations in PTSD converging on the PFC and cerebellum. Whilst PFC alterations are relatively well established in PTSD, the cerebellum has not generally been considered a key region in PTSD. Our findings add to a growing evidence base implicating cerebellar involvement in the pathophysiology of PTSD.


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