Activity In Anterior Cingulate Cortex Research Articles

Emotion Sensitivity of the Error-Related Negativity in Hoarding Individuals

Emerging research suggests that hoarding individuals display atypical activation in their anterior cingulate cortex (ACC). Hemodynamic studies have found a biphasic pattern of ACC activity in hoarding individuals that appears sensitive to possession-related decision-making. Electrophysiological studies suggest that hoarding individuals display a blunted error-related negativity (ERN); an event-related potential originating from the ACC that indexes error-detection. These neural abnormalities may reflect an error sensitivity in hoarding individuals as they acquire and discard, however it may also reflect the hyper-emotionality often reported by individuals who hoard. The present study aimed to examine the emotional sensitivity of the error-related negativity in hoarding individuals outside a possession-related context. Seventeen hoarding individuals and 16 healthy controls underwent continuous electroencephalography (EEG) as they completed Go/No-Go (GNGT) tasks design to elicit the ERN. Identical GNGT tasks were completed both before and after watching a negative mood induction video, and self-reported distress was measured throughout. Neither group displayed any neural effect of the negative mood induction, however the hoarding group displayed a pattern of blunted ERN consistent with previous research. This study provides additional evidence that hoarding individuals display blunted indices of error-detection outside possession-related decision-making. Future research could explore if this reflects a pathophysiology shared with other psychiatric disorders that feature a blunted ERN, and if error-detection is also abnormal as hoarding individuals acquire and discard their possessions.

Combined TMS-EEG-fMRI. The level of TMS-evoked activation in anterior cingulate cortex depends on timing of TMS delivery relative to frontal alpha phase

Synchronizing rTMS pulse delivery to instantaneous electroencephalogram (EEG) rhythms may increase efficacy of rTMS, but few studies have investigated this relationship. Here, we used simultaneous TMS-EEG-fMRI to investigate how ongoing brain activity in DLPFC shapes TMS-evoked responses in the anterior cingulate cortex (ACC) on a trial-by-trial basis.

A single dose of fluoxetine reduces neural limbic responses to anger in depressed adolescents

Depression in adolescence is frequently characterised by symptoms of irritability. Fluoxetine is the antidepressant with the most favourable benefit:risk ratio profile to treat adolescent depression, but the neural mechanisms underlying antidepressant drugs in the young brain are still poorly understood. Previous studies have characterised the neural effects of long-term fluoxetine treatment in depressed adolescents, but these are limited by concurrent mood changes and a lack of placebo control. There is also recent evidence suggesting that fluoxetine reduces the processing of anger in young healthy volunteers, which is consistent with its effect for the treatment of irritability in this age group, but this remains to be investigated in depressed adolescents. Here we assessed the effects of a single, first dose of 10 mg fluoxetine vs. placebo on neural response to anger cues using fMRI in a sample of adolescents with Major Depressive Disorder (MDD) who had been recently prescribed fluoxetine. As predicted, adolescents receiving fluoxetine showed reduced activity in response to angry facial expressions in the amygdala-hippocampal region relative to placebo. Activity in the dorsal anterior cingulate cortex (dACC) was also increased. No changes in symptoms were observed. These results demonstrate, for the first time in depressed adolescents, that fluoxetine has immediate neural effects on core components of the cortico-limbic circuitry prior to clinical changes in mood. The effect on anger is consistent with our previous work and could represent a key mechanism through which fluoxetine may act to alleviate irritability symptoms in adolescent depression.

Dynamic Causal Modeling of Insular, Striatal, and Prefrontal Cortex Activities During a Food-Specific Go/NoGo Task

BackgroundThis study aimed to investigate the dynamic interactions among three neural systems that are implicated in substance and behavioral addictions in response to food cues in young adults. These include an impulsive system involving the striatum, a reflective system involving the prefrontal cortex, and a homeostasis sensing system involving the insular cortex. MethodsCollege students (N = 45) with various levels of body mass index were recruited. Functional magnetic resonance imaging data were acquired while participants performed food-related Go/NoGo tasks, with low-calorie and high-calorie food cues. Participants were scanned under both food satiety and deprivation conditions. Dynamic causal modeling was applied to the data to examine the causal architecture of coupled or distributed dynamics among the aforementioned systems. ResultsParticipants showed difficulty inhibiting responses to high-calorie foods as suggested by higher false alarm rate and decision bias for low-calorie food Go task. This difficulty was enhanced during the food deprivation condition. Deprivation increased neural activity of both the insula and the striatum bilaterally in response to high-calorie foods during Go trials and anterior cingulate cortex and dorsolateral prefrontal cortex activity during NoGo trials. Dynamic causal modeling analysis revealed that food deprivation modulated the communications between the insula, striatum, and dorsolateral prefrontal cortex, and the modulations were positively associated with body mass index. ConclusionsThe results support tripartite views of decision making. Deprivation states, such as hunger, trigger insular activity, which modulates the balance between impulsive and reflective systems when facing tempting food cues.

Modulation of anterior cingulate cortex reward and penalty signalling in medication-naive young-adult subjects with depressive symptoms following acute dose lurasidone.

Aberrations in reward and penalty processing are implicated in depression and putatively reflect altered dopamine signalling. This study exploits the advantages of a placebo-controlled design to examine how a novel D2 antagonist with adjunctive antidepressant properties modifies activity in the brain's reward network in depression. We recruited 43 medication-naïve subjects across the range of depression severity (Beck's Depression Inventory-II score range: 0-43), including healthy volunteers, as well as people meeting full-criteria for major depressive disorder. In a double-blind placebo-controlled cross-over design, all subjects received either placebo or lurasidone (20 mg) across two visits separated by 1 week. Functional magnetic resonance imaging with the Monetary Incentive Delay (MID) task assessed reward functions via neural responses during anticipation and receipt of gains and losses. Arterial spin labelling measured cerebral blood flow (CBF) at rest. Lurasidone altered fronto-striatal activity during anticipation and outcome phases of the MID task. A significant three-way Medication-by-Depression severity-by-Outcome interaction emerged in the anterior cingulate cortex (ACC) after correction for multiple comparisons. Follow-up analyses revealed significantly higher ACC activation to losses in high- v. low depression participants in the placebo condition, with a normalisation by lurasidone. This effect could not be accounted for by shifts in resting CBF. Lurasidone acutely normalises reward processing signals in individuals with depressive symptoms. Lurasidone's antidepressant effects may arise from reducing responses to penalty outcomes in individuals with depressive symptoms.

Longitudinal FDG-PET scan study of brain changes in mice with cancer-induced bone pain and after morphine analgesia.

Morphine is the most commonly used drug for treating physical and psychological suffering caused by advanced cancer. Although morphine is known to elicit multiple supraspinal analgesic effects, its behavioral correlates with respect to the whole-brain metabolic activity during cancer-induced bone pain have not been elucidated. We injected 4T1 mouse breast cancer cells into the left femur bone marrow cavity of BALB/c mice. All mice developed limb use deficits, mechanical allodynia, and hypersensitivity to cold, which were effectively suppressed with morphine. Serial 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) was performed for each mouse before cancer induction (0 day), after cancer-induced bone pain was established (14 days), and during effective morphine treatment (16 days). The longitudinal FDG-PET imaging analysis demonstrated that cancer-induced bone pain increased glucose uptake in the insular cortex and hypothalamus and decreased the activity of the retrosplenial cortex. Morphine reversed the activation of the insular cortex and hypothalamus. Furthermore, morphine activated the amygdala and rostral ventromedial medulla and suppressed the activity of anterior cingulate cortex. Our findings of hypothalamic and insular cortical activation support the hypothesis that cancer-induced bone pain has strong inflammatory and affective components in freely moving animals. Morphine may provide descending inhibitory and facilitatory actions in the treatment of cancer-induced bone pain in a clinical setting.

Expectation of sexual images of adults and children elicits differential dorsal anterior cingulate cortex activation in pedophilic sexual offenders and healthy controls.

BackgroundPedophilic disorder is characterized by increased sexual interest towards children, with comparatively lesser interest towards adults. In real life, the behavior of subjects with pedophilic disorder is shaped by evaluative processes in response to sexually relevant cues. Therefore, brain activation during anticipation of sexually relevant cues is of potential interest. Whereas previous research demonstrated reduced activation when viewing adult (non-preferred) sexual stimuli in pedophilic sex offenders (PSOs), it is not known if anticipation of preferred versus unpreferred stimuli will elicit differential brain activation.MethodsTwo fMRI studies (1.5 and 7 Tesla) were conducted in separate samples, each with 26 subjects (13/13 PSOs/controls) to assess brain activity during expectancy of subsequent adult (non-preferred) sexual stimuli. In the second study (7 Tesla) additionally child (preferred) cues were presented.ResultsAs predicted, expectancy of adult sexual stimuli generated smaller dorsal anterior cingulate cortex (dACC) activation in PSOs in both studies, driven by stronger activation during expectancy of adult erotic stimuli in non-pedophilic controls (HCs). In the second study, PSOs showed significantly increased activations in dACC during expectancy of child stimuli compared with expectancy of adult stimuli. This difference was significantly greater compared to the same contrast in HCs, thus demonstrating preference specificity of dACC activation.ConclusionOur findings support the notion of decreased brain activation to adult cues in PSOs and preference specificity in neural response during expectancy of erotic stimuli. The localization of these cue reactivity differences in the salience network supports the interpretation that PSOs show abnormally increased preparatory activation even before relevant sexual stimuli are actually presented.

Low-dose augmentation with buprenorphine increases emotional reactivity but not reward activity in treatment resistant mid- and late-life depression.

Buprenorphine is currently being studied for treatment-resistant depression because of its rapid effect, relative safety, and unique pharmacodynamics. To understand the neural impact of buprenorphine in depression, we examined acute limbic and reward circuit changes during an intervention with low-dose buprenorphine augmentation pharmacotherapy. Mid and late-life adults with major depression (N = 31) who did not completely respond to an adequate trial of venlafaxine were randomized to augmentation with low-dose buprenorphine or matching placebo. We investigated early neural changes using functional magnetic resonance imaging (fMRI) from pre-randomization to 3 weeks using both an emotional reactivity task and a gambling task. We tested if: 1) there were significant neural changes acutely per intervention group, and 2) if acute neural changes were associated with depressive symptom change over 8 weeks using both the total score and the dysphoria subscale of the Montgomery Asberg Depression Rating Scale. Participants in both the buprenorphine and placebo groups showed similar changes in depressive symptoms. Neither the emotional reactivity nor gambling task resulted in significant neural activation changes from pre-randomization to 3-weeks. In both groups, increases in rostral anterior cingulate (rACC) and ventromedial prefrontal cortex (vmPFC) activation during the emotional reactivity task were associated with overall symptom improvement. In the buprenorphine but not the placebo group, increased activation in left anterior insula (aINS) and bilateral middle frontal gyrus (MFG) was associated with improvement on the dysphoria subscale. Activation changes in the reward task were not associated with buprenorphine. This is the first study to show an association between acute neural changes during emotion reactivity and changes in depression severity with buprenorphine treatment.

Childhood adversity, externalizing behavior, and substance use in adolescence: Mediating effects of anterior cingulate cortex activation during inhibitory errors.

Childhood adversity can negatively impact development across various domains, including physical and mental health. Adverse childhood experiences have been linked to aggression and substance use; however, developmental pathways to explain these associations are not well characterized. Understanding early precursors to later problem behavior and substance use can inform preventive interventions. The aim of the current study was to examine neurobiological pathways through which childhood adversity may lead to early adolescent problem behavior and substance use in late adolescence by testing two prospective models. Our first model found that early adolescent externalizing behavior mediates the association between childhood adversity and alcohol, cigarette, and marijuana use in late adolescence. Our second model found that activation in the anterior cingulate cortex (ACC) during an inhibitory control task mediates the association between childhood adversity and early adolescent externalizing behavior, with lower ACC activation associated with higher levels of adversity and more externalizing behavior. Together these findings indicate that the path to substance use in late adolescence from childhood adversity may operate through lower functioning in the ACC related to inhibitory control and externalizing behavior. Early life stressors should be considered an integral component in the etiology and prevention of early and problematic substance use.

Reward-circuit biomarkers of risk and resilience in adolescent depression.

Dysfunctional reward processing is a core feature of major depressive disorder. While there is growing knowledge of reward processing in adolescent depression, researchers have ignored neural mechanisms of resilience to depression. Here, we examine neural correlates of reward processing that characterize resilience and risk in adolescents at risk for depression, facilitating the development of effective intervention approaches that strengthen resilience to psychopathology in at-risk youth. 50 adolescent females were followed through age 18: 32 at-risk adolescents who either did (remitted-depressed; n = 15) or did not (resilient; n = 17) experience a depressive episode, and 18 low-risk healthy controls. Participants completed clinical assessments at 18-month intervals and an fMRI reward-processing task in late adolescence. We conducted predictive modeling with a priori reward regions of interest (ROIs). At-risk resilient and remitted-depressed adolescents exhibited less striatal activation than did controls during anticipation of reward. Resilient adolescents exhibited greater activation than did remitted-depressed adolescents in the middle frontal gyrus during reward anticipation, and less activation in the superior frontal gyrus and cuneus during processing of reward outcome. Using predictive modeling, ventral anterior cingulate cortex and putamen activation during reward processing distinguished resilient from remitted-depressed adolescents with 83% accuracy. The relatively small sample size of only females and the fact that fMRI data were obtained at one time point in late adolescence are limitations. Distinct patterns of neural activation in reward circuitry appear to be markers of risk and resilience that may be targets for prevention and treatment approaches aimed at strengthening adaptive reward processing in at-risk adolescents.

Pretreatment Rostral Anterior Cingulate Cortex Connectivity With Salience Network Predicts Depression Recovery: Findings From the EMBARC Randomized Clinical Trial

BackgroundBaseline rostral anterior cingulate cortex (rACC) activity is a well-replicated nonspecific predictor of depression improvement. The rACC is a key hub of the default mode network, which prior studies indicate is hyperactive in major depressive disorder. Because default mode network downregulation is reliant on input from the salience network and frontoparietal network, an important question is whether rACC connectivity with these systems contributes to depression improvement. MethodsOur study evaluated this hypothesis in outpatients (N = 238; 151 female) enrolled in the Establishing Moderators and Biosignatures of Antidepressant Response for Clinical Care (EMBARC) 8-week randomized clinical trial of sertraline versus placebo for major depressive disorder. Depression severity was measured using the Hamilton Rating Scale for Depression, and electroencephalography was recorded at baseline and week 1. Exact low-resolution electromagnetic tomography was used to compute activity from the rACC, and key regions within the default mode network (posterior cingulate cortex), frontoparietal network (left dorsolateral prefrontal cortex), and salience network (right anterior insula [rAI]). Connectivity in the theta band (4.5–7 Hz) and beta band (12.5–21 Hz) was computed using lagged phase synchronization. ResultsStronger baseline theta-band rACC–rAI (salience network hub) connectivity predicted greater depression improvement across 8 weeks of treatment for both treatment arms (B = −0.57, 95% confidence interval = −1.07, −0.08, p = .03). Early increases in theta-band rACC–rAI connectivity predicted greater likelihood of achieving remission at week 8 (odds ratio = 2.90, p = .03). ConclusionsAmong patients undergoing treatment, theta-band rACC–rAI connectivity is a prognostic, albeit treatment-nonspecific, indicator of depression improvement, and early connectivity changes may predict clinically meaningful outcomes.

Emotionally Aversive Cues Suppress Neural Systems Underlying Optimal Learning in Socially Anxious Individuals.

Learning and decision-making are modulated by socio-emotional processing and such modulation is implicated in clinically relevant personality traits of social anxiety. The present study elucidates the computational and neural mechanisms by which emotionally aversive cues disrupt learning in socially anxious human individuals. Healthy volunteers with low or high trait social anxiety performed a reversal learning task requiring learning actions in response to angry or happy face cues. Choice data were best captured by a computational model in which learning rate was adjusted according to the history of surprises. High trait socially anxious individuals used a less-dynamic strategy for adjusting their learning rate in trials started with angry face cues and unlike the low social anxiety group, their dorsal anterior cingulate cortex (dACC) activity did not covary with the learning rate. Our results demonstrate that trait social anxiety is accompanied by disruption of optimal learning and dACC activity in threatening situations.SIGNIFICANCE STATEMENT Social anxiety is known to influence a broad range of cognitive functions. This study tests whether and how social anxiety affects human value-based learning as a function of uncertainty in the learning environment. The findings indicate that, in a threatening context evoked by an angry face, socially anxious individuals fail to benefit from a stable learning environment with highly predictable stimulus-response-outcome associations. Under those circumstances, socially anxious individuals failed to use their dorsal anterior cingulate cortex, a region known to adjust learning rate to environmental uncertainty. These findings open the way to modify neurobiological mechanisms of maladaptive learning in anxiety and depressive disorders.

Neuroimaging Correlates of Resilience to Traumatic Events-A Comprehensive Review.

Improved understanding of the neurobiological correlates of resilience would be an important step toward recognizing individuals at risk of developing post-traumatic stress disorder (PTSD) or other trauma-related diseases, enabling both preventative measures and individually tailored therapeutic approaches. Studies on vulnerability factors allow drawing conclusions on resilience. Structural changes of cortical and subcortical structures, as well as alterations in functional connectivity and functional activity, have been demonstrated to occur in individuals with PTSD symptoms. Relevant areas of interest are hippocampus, amygdala, insula, anterior cingulate cortex, and prefrontal cortex, as well as related brain networks, such as the default-mode, salience, and central executive network. This review summarizes the existing literature and integrates findings from cross-sectional study designs with two-group designs (trauma exposed individuals with and without PTSD), three-group designs (with an additional group of unexposed, healthy controls), twin-studies and longitudinal studies. In terms of structural findings, decreased hippocampal volume in PTSD individuals might be either a vulnerability factor or a result of trauma exposure, or both. Reduced anterior cingulate cortex and prefrontal cortex volumes seem to be predisposing factors for increased vulnerability. Regarding functional connectivity, increased amygdala connectivity has been demonstrated selectively in PTSD individuals, as well as increased default-mode-network and salience network connectivity. In terms of functional activity, increased amygdala and anterior cingulate cortex activities, and decreased prefrontal cortex activity as a response to external stimuli have been associated with higher vulnerability. Increased prefrontal cortex activity seemed to be a protective factor. Selecting adequate study designs, optimizing the diagnostic criteria, as well as differentiating between types of trauma and accounting for other factors, such as gender-specific differences, would be well-served in future research. Conclusions on potential preventative measures, as well as clinical applications, can be drawn from the present literature, but more studies are needed.

Roles of Ventromedial Prefrontal Cortex and Anterior Cingulate in Subjective Valuation of Prospective Effort.

The perceived effort level of an action shapes everyday decisions. Despite the importance of these perceptions for decision-making, the behavioral and neural representations of the subjective cost of effort are not well understood. While a number of studies have implicated anterior cingulate cortex (ACC) in decisions about effort/reward trade-offs, none have experimentally isolated effort valuation from reward and choice difficulty, a function that is commonly ascribed to this region. We used functional magnetic resonance imaging to monitor brain activity while human participants engaged in uncertain choices for prospective physical effort. Our task was designed to examine effort-based decision-making in the absence of reward and separated from choice difficulty-allowing us to investigate the brain's role in effort valuation, independent of these other factors. Participants exhibited subjectivity in their decision-making, displaying increased sensitivity to changes in subjective effort as objective effort levels increased. Analysis of blood-oxygenation-level dependent activity revealed that the ventromedial prefrontal cortex (vmPFC) encoded the subjective valuation of prospective effort, and ACC activity was best described by choice difficulty. These results provide insight into the processes responsible for decision-making regarding effort, partly dissociating the roles of vmPFC and ACC in prospective valuation of effort and choice difficulty.

The influence of the OPRM1 (A118G) polymorphism on behavioral and neural correlates of aggression in healthy males

Current models of aggression suggest that in addition to personality traits and environmental factors, biological vulnerability associated with genetics substantially impacts aggressive behavior. In a functional imaging study, we investigated the influence of the single nucleotide polymorphism of the mu 1 subtype opioid receptor gene (OPRM1), implicated in sociability, on correlates of trait and state aggression to delineate the function of these influences in aggression. A key aim was further to differentiate different aspects of aggressive reactions – namely, the reaction to provocation and the decision to punish an opponent.59 healthy males performed a modified Taylor Aggression Paradigm during functional magnetic resonance imaging. The implementation of the paradigm allowed for individual assessments of the decision to behave aggressively, the experience of provocation and the ramification of punishment for the participant or the opponent. The influence of variation in the OPRM1 gene was measured by the functional A118G polymorphism.G allele carriers showed lower levels of general aggression and self-reported physical aggression. Additionally, these participants exhibited increased activation in dorsolateral prefrontal, orbitofrontal, anterior cingulate and insular cortices when choosing higher punishments for the opponent. The OPRM1 polymorphism did not influence aggression in reaction to social provocation. Thus, we suggest that this genetic variant affects one's trait aggressiveness rather than actual behavioral reactivity to provocation. Investigating brain regions that are specifically linked to provocation yielded activation in cortico-limbic circuits which might mediate the evaluation of provocation and the experience of anger and thus shed light on neural processes underlying the risk for aggressive behavior.This article is part of the Special Issue entitled ‘Current status of the neurobiology of aggression and impulsivity’.

Brain Activity Map Extraction of Neuromyelitis Optica Patients Using Resting-State fMRI Data Based on Amplitude of Low Frequency Fluctuations and Regional Homogeneity Analysis

Introduction: Neuromyelitis Optica (NMO) is a rare inflammatory disease of the central nervous system which generally affecting the spinal cord and optic nerve. Damage to the optic nerve can result in the patient's dim vision or even blindness, while the spinal cord damage may lead to sensory and motor paralysis and the weakness of the lower limbs in the patient. Magnetic Resonance Imaging (MRI) is one of the imaging methods for NMO detection. Recently, the fMRI scans in NMO disease is very common. fMRI is a non-invasive method which uses magnetic technology. fMRI images are related to environmental changes in the blood flow of any brain regions. This imaging method is designed to identify parts of the brain cortex activated for specific tasks, and it is mostly used to carry out neurological studies. Materials and Method: After the initial diagnosis by the neurologist, rest-fMRI imaging was performed on 25 healthy persons as the control group and 25 persons suffering from NMO as the test group. after the data were obtained, the data pre-processing was carried out which included the slice-timing, motion correction, and spatial normalization steps. In order to eliminate the noise and other artifact effects, a band-pass filter was used. Finally, the data were filtered using a Gaussian kernel for the smoothing purposes. The amplitude of low frequency fluctuations (ALFF) and regional homogeneity (ReHo) methods were used to investigate the activity of brain regions. For this purpose, at first, time series associated with each of the brain 3D volume voxels were extracted. After the selection of the brain regions between the two groups, registering the functional images on structural images and the standard atlas, the statistical analysis of the results was carried out. The present research was performed in MATLAB using the Resting-State fMRI Data Analysis Toolkit. Results: The statistical comparison of the images of the test and control groups which was obtained from the group analyses of the low frequency fluctuations mappings in the resting state pointed to a decrease in the activity of the left Anterior Cingulate Cortex, right precuneus, left Posterior Cingulate Cortex, medial frontal gyrus, and right middle temporal gyrus regions. On the other hand, there was observed an increase in the activity of right inferior frontal gyrus and left thalamus regions. Conclusion: The findings in the data associated with fMRI images in NMO patients, showed an abnormal brain activity in the regions associated with cognitive, optic, and motor tasks. This may be because of the consistency of the brain with functional disorder in NMO subjects as well as the compensation of this pathophysiological disorder by the other parts of the brain.

Enhanced Remote Long-Term Social Memory Despite an Absence of Any Recent Long-Term Memory for That Same Event

System consolidation (SC) is a process by which memories initially require the hippocampus for recent long-term memory (LTM) but then become increasingly independent of the hippocampus and more dependent on the cortex for remote LTM. Here we study the role of phosphodiesterase 11A4 (PDE11A4) in SC. PDE11A4; which degrades cAMP/cGMP and regulates glutamate signaling and protein synthesis; is preferentially expressed in neurons of CA1; the subiculum; and the adjacently connected amygdalohippocampal region. Deletion of PDE11A enhances remote LTM for social odor recognition and social transmission of food preference (STFP) despite eliminating/silencing recent LTM for those same social events. Measurement of Arc mRNA; a surrogate marker of neuronal activation; suggests the impaired recent LTM for STFP observed in Pde11 KO mice corresponds with decreased activation of ventral CA1 relative to wild-type (WT) littermates; whereas; the enhanced remote LTM for STFP observed in Pde11a KO mice corresponds with increased activation and altered functional connectivity of anterior cingulate cortex; frontal association cortex; parasubiculum; and the superficial layer of medial entorhinal cortex. The apparent increased neural activation observed in prefrontal cortex of Pde11a KO mice may be related to an upregulation of the NMDA receptor subunits NR1 and NR2A. Viral restoration of PDE11A4 to vCA1 alone is sufficient to reverse both the LTM phenotypes and upregulation of NR1 exhibited by Pde11a KO mice. Together our findings suggest remote LTM can be decoupled from recent LTM and may have relevance for cognitive deficits associated with temporal lobe epilepsy or transient global amnesia.

Effect of corticotropin-releasing hormone receptor1 gene variation on psychosocial stress reaction via the dorsal anterior cingulate cortex in healthy adults

ObjectiveIt has been proposed that the common intronic CRHR1 SNP rs110402 is associated with anxiety and cortisol response patterns and plays a key role in vulnerability to certain mental disorders. The current study explored the effect of rs110402 genotype on psychological stress processing in healthy adults. MethodsThe Montreal Imaging Stress Task (MIST) was administered to 140 healthy adults (34 C carriers and 106 TT homozygotes) during functional magnetic resonance imaging. Between-group differences in self-reported stress level, whole brain activation, and cortisol levels were assessed. ResultsThe rs110402 genotype groups differed in stress-induced cortisol response and bilateral dorsal anterior cingulate cortex (dACC) activity. The TT homozygotes showed greater stress-induced activation in the bilateral dACC compared to C carriers. Interestingly, dACC activity during MIST was negatively correlated with cortisol response in healthy adults. State anxiety, trait anxiety, and mental resilience did not differ between genotypes. ConclusionsCRHR1 SNP rs110402 genotype plays a role in psychosocial neural processing and cortisol response in healthy adults. The activity in dACC may mediate effect of rs110402 on psychosocial stress processing in the healthy population. Moreover, level of dACC activation may be associated with stress vulnerability.

Decisions and their future implications

Neuroscience We constantly make choices. It is often important to consider not only the short-term but also the longer-term implications of a choice, also known as its prospective value. In a combined decision-making and brain-scanning study, Kolling et al. found that when humans make sequential decisions, they do not only consider their immediately available options. Instead, they incorporate the average value of future options, their variability, and the time frame or search horizon, as well as search costs. Furthermore, humans even consider individual capacities and preferences for making decisions in the future. Brain activity in the dorsal anterior cingulate cortex represents prospective value, but when there is an increased need to overcome costs, activity in the ventral striatum and perigenual anterior cingulate cortex is more strongly coupled. Neuron 99 , 1069 (2018).

Neural correlates of body comparison and weight estimation in weight-recovered anorexia nervosa: a functional magnetic resonance imaging study

BackgroundThe neural mechanisms underlying body dissatisfaction and emotional problems evoked by social comparisons in patients with anorexia nervosa (AN) are currently unclear. Here, we elucidate patterns of brain activation among recovered patients with AN (recAN) during body comparison and weight estimation with functional magnetic resonance imaging (fMRI).MethodsWe used fMRI to examine 12 patients with recAN and 13 healthy controls while they performed body comparison and weight estimation tasks with images of underweight, healthy weight, and overweight female bodies. In the body comparison task, participants rated their anxiety levels while comparing their own body with the presented image. In the weight estimation task, participants estimated the weight of the body in the presented image. We used between-group region of interest (ROI) analyses of the blood oxygen level dependent (BOLD) signal to analyze differences in brain activation patterns between the groups. In addition, to investigate activation outside predetermined ROIs, we performed an exploratory whole-brain analysis to identify group differences.ResultsWe found that, compared to healthy controls, patients with recAN exhibited significantly greater activation in the pregenual anterior cingulate cortex (pgACC) when comparing their own bodies with images of underweight female bodies. In addition, we found that, compared with healthy controls, patients with recAN exhibited significantly smaller activation in the middle temporal gyrus corresponding to the extrastriate body area (EBA) when comparing their own bodies, irrespective of weight, during self-other comparisons of body shape.ConclusionsOur findings from a group of patients with recAN suggest that the pathology of AN may lie in an inability to regulate negative affect in response to body images via pgACC activation during body comparisons. The findings also suggest that altered body image processing in the brain persists even after recovery from AN.