Tell it to a child! A brain stimulation study of the role of left inferior frontal gyrus in emotion regulation during storytelling

Urgesi, Cosimo; Mattiassi, Alan D. A.; Buiatti, Tania; Marini, Andrea

doi:10.1016/j.neuroimage.2016.05.039

Cited by 23 publications

(12 citation statements)

References 61 publications

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“…Indeed, in a previous fMRI study, participants exerted self control by performing thought suppression (or not, as a control) before being engaged in a Stroop task (Luethi et al, 2016). Compared to control, participants performed worse on the Stroop task along with decreased left IFC activation, suggesting that left IFC activity may reflect effort and arousal (Urgesi et al, 2016) that is required across different behavioral challenges. Also in support of a role of the left IFC in sustaining attention and effort were imaging studies reporting a detrimental effect of its signal variability on cognitive stability, as shown in increased response time costs during distractor inhibition (Armbruster-Genc et al, 2016) and increased switch cost in a switching task in association with less functional connectivity of the left IFC (Yin et al, 2015).…”

Section: Discussionmentioning

confidence: 97%

Distinct neural processes support post-success and post-error slowing in the stop signal task

et al. 2017

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Executive control requires behavioral adaptation to environmental contingencies. In the stop signal task (SST), participants exhibit slower go trial reaction time (RT) following a stop trial, whether or not they successfully interrupt the motor response. In previous fMRI studies, we demonstrated activation of the right-hemispheric ventrolateral prefrontal cortex, in the area of inferior frontal gyrus, pars opercularis (IFGpo) and anterior insula (AI), during post-error slowing (PES). However, in similar analyses we were not able to identify regional activities during post-success slowing (PSS). Here, we revisited this issue in a larger sample of participants (n=100) each performing the SST for 40 min during fMRI. We replicated IFGpo/AI activation to PES (p≤0.05, FWE corrected). Further, PSS engages decreased activation in a number of cortical regions including the left inferior frontal cortex (IFC; p≤0.05, FWE corrected). We employed Granger causality mapping to identify areas that provide inputs each to the right IFGpo/AI and left IFC, and computed single-trial amplitude (STA) of stop trials of these input regions as well as the STA of post-stop trials of the right IFGpo/AI and left IFC. The STAs of the right inferior precentral sulcus and supplementary motor area (SMA) and right IFGpo/AI were positively correlated and the STAs of the left SMA and left IFC were positively correlated (slope>0, p's≤0.01, one-sample t test), linking regional responses during stop success and error trials to those during PSS and PES. These findings suggest distinct neural mechanisms to support PSS and PES.

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Section: Discussionmentioning

confidence: 97%

Distinct neural processes support post-success and post-error slowing in the stop signal task

et al. 2017

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“…Gray matter reductions extended to the rIFG, an adjacent neural structure implicated in both emotion- and self-regulation, particularly in social contexts (Grecucci et al, 2013; Kohn et al, 2014; Urgesi, Mattiassi, Buiatti, & Marini, 2016). Lesions to this region result in impaired behavioral inhibition and impulsive decision making (Aron, Robbins, & Poldrack, 2004; Chamberlain & Sahakian, 2007).…”

Section: Discussionmentioning

confidence: 99%

Self-injuring adolescent girls exhibit insular cortex volumetric abnormalities that are similar to those seen in adults with borderline personality disorder

et al. 2018

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Self-inflicted injury (SII) in adolescence is a serious public health concern that portends prospective vulnerability to internalizing and externalizing psychopathology, borderline personality development, suicide attempts, and suicide. To date, however, our understanding of neurobiological vulnerabilities to SII is limited. Behaviorally, affect dysregulation is common among those who self-injure. This suggests ineffective cortical modulation of emotion, as observed among adults with borderline personality disorder. In borderline samples, structural and functional abnormalities are observed in several frontal regions that subserve emotion regulation (e.g., anterior cingulate, insula, dorsolateral prefrontal cortex). However, no volumetric analyses of cortical brain regions have been conducted among self-injuring adolescents. We used voxel-based morphometry to compare cortical gray matter volumes between self-injuring adolescent girls, ages 13–19 years (n = 20), and controls (n = 20). Whole-brain analyses revealed reduced gray matter volumes among self-injurers in the insular cortex bilaterally, and in the right inferior frontal gyrus, an adjacent neural structure also implicated in emotion and self-regulation. Insular and inferior frontal gyrus gray matter volumes correlated inversely with self-reported emotion dysregulation, over-and-above effects of psychopathology. Findings are consistent with an emotion dysregulation construal of SII, and indicate structural abnormalities in some but not all cortical brain regions implicated in borderline personality disorder among adults.

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“…The inferior frontal gyrus (IFG) is a brain area involved in semantic unification, emotion perception and regulation and processing of negative emotional stimuli ( Etkin et al, 2011 ; Zhu et al, 2012 ; Tabei, 2015 ; Urgesi et al, 2016 ). This suggests that activation of this brain area during Ayahuasca ingestion could be involved in the processing of trauma.…”

Section: Ayahuasca Ingestion Modulates Brain Activitymentioning

confidence: 99%

“…Given that Ayahuasca ingestion (a) hyperactivates brain areas involved in the retrieval of memories (parahippocampal gyrus), regulation of emotional processing and perception of errors (anterior insula), regulation and processing of negative emotional stimuli (IFG) and emotional arousal (amygdala), and (b) boosts dopaminergic neurotransmission, an essential requisite for memory retrieval and reconsolidation, I postulate that Ayahuasca creates a pattern of brain activity which is conducive to the recall and/or re-experiencing of traumatic memories, or memories that have a negative connotation ( Phillips et al, 1998 ; Ullsperger et al, 2010 ; Etkin et al, 2011 ; Zhu et al, 2012 ; Tabei, 2015 ; Urgesi et al, 2016 ). This process is assisted by the anti-amnesic effects of SIGMAR1 activation, which are potentially mediated by enhanced cholinergic, NMDA-glutamatergic and dopaminergic neurotransmission and might be involved in the retrieval of repressed memories ( Earley et al, 1991 ; Maurice et al, 1998 ; Antonini et al, 2009 ).…”

Section: Hypothesis: Ayahuasca Reconsolidates Traumatic Memories Via mentioning

confidence: 99%

Hypothesis: The Psychedelic Ayahuasca Heals Traumatic Memories via a Sigma 1 Receptor-Mediated Epigenetic-Mnemonic Process

Inserra

2018

Front. Pharmacol.

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Ayahuasca ingestion modulates brain activity, neurotransmission, gene expression and epigenetic regulation. N,N-Dimethyltryptamine (DMT, one of the alkaloids in Ayahuasca) activates sigma 1 receptor (SIGMAR1) and others. SIGMAR1 is a multi-faceted stress-responsive receptor which promotes cell survival, neuroprotection, neuroplasticity, and neuroimmunomodulation. Simultaneously, monoamine oxidase inhibitors (MAOIs) also present in Ayahuasca prevent the degradation of DMT. One peculiarity of SIGMAR1 activation and MAOI activity is the reversal of mnemonic deficits in pre-clinical models. Since traumatic memories in post-traumatic stress disorder (PTSD) are often characterised by “repression” and PTSD patients ingesting Ayahuasca report the retrieval of such memories, it cannot be excluded that DMT-mediated SIGMAR1 activation and the concomitant MAOIs effects during Ayahuasca ingestion might mediate such “anti-amnesic” process. Here I hypothesise that Ayahuasca, via hyperactivation of trauma and emotional memory-related centres, and via its concomitant SIGMAR1- and MAOIs- induced anti-amnesic effects, facilitates the retrieval of traumatic memories, in turn making them labile (destabilised). As Ayahuasca alkaloids enhance synaptic plasticity, increase neurogenesis and boost dopaminergic neurotransmission, and those processes are involved in memory reconsolidation and fear extinction, the fear response triggered by the memory can be reprogramed and/or extinguished. Subsequently, the memory is stored with this updated significance. To date, it is unclear if new memories replace, co-exist with or bypass old ones. Although the mechanisms involved in memory are still debated, they seem to require the involvement of cellular and molecular events, such as reorganisation of homo and heteroreceptor complexes at the synapse, synaptic plasticity, and epigenetic re-modulation of gene expression. Since SIGMAR1 mobilises synaptic receptor, boosts synaptic plasticity and modulates epigenetic processes, such effects might be involved in the reported healing of traumatic memories in PTSD patients. If this theory proves to be true, Ayahuasca could come to represent the only standing pharmacological treatment which targets traumatic memories in PTSD. Lastly, since SIGMAR1 activation triggers both epigenetic and immunomodulatory programmes, the mechanism here presented could help understanding and treating other conditions in which the cellular memory is dysregulated, such as cancer, diabetes, autoimmune and neurodegenerative pathologies and substance addiction.

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Tell it to a child! A brain stimulation study of the role of left inferior frontal gyrus in emotion regulation during storytelling

Cited by 23 publications

References 61 publications

Distinct neural processes support post-success and post-error slowing in the stop signal task

Distinct neural processes support post-success and post-error slowing in the stop signal task

Self-injuring adolescent girls exhibit insular cortex volumetric abnormalities that are similar to those seen in adults with borderline personality disorder

Hypothesis: The Psychedelic Ayahuasca Heals Traumatic Memories via a Sigma 1 Receptor-Mediated Epigenetic-Mnemonic Process

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