From anatomy to function: the role of the somatosensory cortex in emotional regulation

Kropf, Erika; Syan, Sabrina K.; Minuzzi, Luciano; Frey, Benício N.

doi:10.1590/1516-4446-2018-0183

Cited by 214 publications

(164 citation statements)

References 57 publications

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“…(3) Leptin mediated both the association between ReHo alterations (primary somatosensory and visual association cortices) and core depressive symptoms as well as BMI. These findings are consistent with an expanding literature implicating primary somatosensory cortex 5,38,39 , visual association cortex 40,41 and leptin 25,42 in depression and further suggesting that depressive symptoms are dimensional features across MPDs. Utilising a transdiagnostic approach, the extent of overlap and distinct alterations in ReHo values among SCZ, BPD and MDD were examined.…”

Section: Discussionsupporting

confidence: 90%

“…Consistent with a previous study 18 , we observed ReHo alterations in primary sensory, visual association and orbital frontal cortices associated with depressive symptoms. The abovementioned brain regions are involved in emotion processing [38][39][40]47 . Primary somatosensory and visual association cortices play important roles in encoding somatosensory sensations and emotional recognition and regulation 39 .…”

Section: Discussionmentioning

confidence: 99%

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Applying dimensional psychopathology: transdiagnostic associations among regional homogeneity, leptin and depressive symptoms

et al. 2020

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Dimensional psychopathology and its neurobiological underpinnings could provide important insights into major psychiatric disorders, including major depressive disorder, bipolar disorder and schizophrenia. In a dimensional transdiagnostic approach, we examined depressive symptoms and their relationships with regional homogeneity and leptin across major psychiatric disorders. A total of 728 participants (including 403 patients with major psychiatric disorders and 325 age-gender-matched healthy controls) underwent resting-state functional magnetic resonance imaging at a single site. We obtained plasma leptin levels and depressive symptom measures (Hamilton Depression Rating Scale (HAMD)) within 24 h of scanning and compared the regional homogeneity (ReHo), plasma leptin levels and HAMD total score and factor scores between patients and healthy controls. To reveal the potential relationships, we performed correlational and mediational analyses. Patients with major psychiatric disorders had significant lower ReHo in primary sensory and visual association cortices and higher ReHo in the frontal cortex and angular gyrus; plasma leptin levels were also elevated. Furthermore, ReHo alterations, leptin and HAMD factor scores had significant correlations. We also found that leptin mediated the transdiagnostic relationships among ReHo alterations in primary somatosensory and visual association cortices, core depressive symptoms and body mass index. The transdiagnostic associations we demonstrated support the common neuroanatomical substrates and neurobiological mechanisms. Moreover, leptin could be an important association among ReHo, core depressive symptoms and body mass index, suggesting a potential therapeutic target for dimensional depressive symptoms across major psychiatric disorders.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Applying dimensional psychopathology: transdiagnostic associations among regional homogeneity, leptin and depressive symptoms

et al. 2020

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“…Component-1 showed a ventral-to dorsal gene expression pattern that was associated with higher correlations between CT and clinical scores, namely, the mental state of Parkinson's disease patients and the performance of motor functions. The pathways involved in ER-Golgi traffic were notably high expressed in the postcentral gyrus which contains the somatosensory cortex that is known for its role in processing sensory information and the regulation of emotion (Kropf et al, 2019). Our results suggest that genes in ER-Golgi traffic pathways are important for cognitive functions controlled by the postcentral gyrus.…”

Section: Discussionmentioning

confidence: 58%

Transcriptomic signatures associated with regional cortical thickness changes in Parkinson’s disease

Keo

Dzyubachyk

Hilten

et al. 2020

Preprint

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Cortical atrophy is a common manifestation in Parkinson's disease, particularly in later disease stages. Here, we investigated patterns of cortical thickness using T1-weighted anatomical MRI data of 149 Parkinson's disease patients and 369 controls. To elucidate the molecular underpinnings of cortical thickness changes in Parkinson's disease, we performed an integrated analysis of brain-wide healthy transcriptomic data from the Allen Human Brain Atlas and neuroimaging features. For this purpose, we used partial least squares regression to identify gene expression patterns correlated with cortical thickness changes. In addition, we identified gene expression patterns underlying the relationship between cortical thickness and clinical domains of Parkinson's disease. Our results show that genes whose expression in the healthy brain is associated with cortical thickness changes in Parkinson's disease are enriched in biological pathways related to sumoylation, regulation of mitotic cell cycle, mitochondrial translation, DNA damage responses, and ER-Golgi traffic. The associated pathways were highly related to each other and all belong to cellular maintenance mechanisms. The expression of genes within most pathways was negatively correlated with cortical thickness changes, showing higher expression in regions associated with decreased cortical thickness (atrophy). On the other hand, sumoylation pathways were positively correlated with cortical thickness changes, showing higher expression in regions with increased cortical thickness (hypertrophy). Our findings suggest that alterations in the balanced interplay of these mechanisms play a role in changes of cortical thickness in Parkinson's disease and possibly influence motor and cognitive functions. Abbreviations: AHBA = Allen Human Brain Atlas; CT = cortical thickness; LED = levodopa equivalent dose; MDS-UPDRS = Movement Disorder Society-sponsored revision of the unified Parkinson's disease rating scale; MMSE = mini-mental state examination; PLS = partial least squares; SENS-PD = severity of non-dopaminergic symptoms in Parkinson's disease Running title: Gene expression and cortical thickness

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“…In particular, the SI participates in processing emotional significance, emotion regulation and in the generation of the emotion of fear (71).…”

Section: Discussionmentioning

confidence: 99%

Offline tDCS modulates prefrontal-cortical-subcortical-cerebellar fear pathways in delayed fear extinction

Ganho-Ávila

Guiomar

Valério

et al. 2019

Preprint

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Transcranial direct current stimulation (tDCS) has been studied as an add-on enhancer of extinction-based treatments for anxiety disorders. However, previous studies have failed to address one issue of translational significance: the to-be extinguished fear memory must be consolidated. Additionally, extant literature shows conflicting results about the anxiolytic effect of tDCS delivered to the right dorsolateral prefrontal cortex. To address these issues, we recruited thirty-four female participants to participate in a two-day fear conditioning procedure. On Day 1, laboratory fear acquisition was confirmed by self-reported contingency ratings. On Day 2, participants were randomly assigned to either the control group (n=18; completed the extinction session) or the tDCS group (n=16; whom received 20min tDCS session of 1mA [cathode -F4; anode -contralateral deltoid immediately before extinction).Functional magnetic resonance imagining data showed that tDCS modulates the late phase of the delayed extinction process. In particular, neural activity of the frontal middle cortex, the left frontal superior cortex, and the left and right paracentral and postcentral cortices is increased during the processing of the CS-, supporting the processing of uncertainty. Furthermore, during the processing of threat, tDCS leads to an increased information flow from the contralateral prefrontal cortex along the cortical-amygdalo-hippocampalcerebellar pathways. Thus, the boosted processing of uncertainty and the stronger coupling during threat processing might well be the mechanisms by which tDCS boosts stimuli discrimination, leading to decreased symptoms and enhanced clinical gains.Running head: Using tDCS to interfere with fear extinction Running head: Using tDCS to interfere with fear extinction of anxiety symptoms. According to this model, the fear response is elicited by environmental threats through an associative learning whereby the neutral stimulus (conditioned stimulus, CS+) is paired with an aversive stimulus (unconditioned stimulus, US) and a danger predicting value is assigned to it, eliciting the conditioned fear response (CR; 14). A deregulated fear response may lead to incorrect detection of danger and sustained anxiety-related symptoms (e.g. hyper-vigilance and excessive worrying). Thus, to eliminate the consolidated CR, extinction (the translational equivalent to exposure-based therapies) is implemented, consisting of consecutive presentations of the CS+ alone, leading to a new learning that inhibits the CS+/US association (18).By delivering tDCS to the right or left DLPFC to enhance fear extinction, researchers aimed to artificially modulate brain activity and decrease the fear response (19)(20)(21)(22). Counterintuitively, whereas previous studies have shown that tDCS using the anode electrode over the DLPFC leads to decreased fear, this gain was also associated with the adverse effect of decreasing stimuli discrimination (21,23). Differently, using the cathodal electrode over the DLPFC led to no effect in decreas...

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From anatomy to function: the role of the somatosensory cortex in emotional regulation

Cited by 214 publications

References 57 publications

Applying dimensional psychopathology: transdiagnostic associations among regional homogeneity, leptin and depressive symptoms

Applying dimensional psychopathology: transdiagnostic associations among regional homogeneity, leptin and depressive symptoms

Transcriptomic signatures associated with regional cortical thickness changes in Parkinson’s disease

Offline tDCS modulates prefrontal-cortical-subcortical-cerebellar fear pathways in delayed fear extinction

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