Negative Emotional Processing Research Articles

Pictures of preterm infants elicit increased affective responses and reduced reward-motivation or perspective taking in the maternal brain

Preterm-birth increases the risk of several physical, cognitive, neuromotor, and psychosocial problems in children, and is also related to difficulties in the parent–child relationship. Research suggests that the development of early parent–child interactions in general is affected by deviations from typical infant facial characteristics, which may also be important in the case of small, preterm born infants. Therefore, we examined mothers’ (N = 22, of whom 17 had no direct experience with preterm birth) neural responses to pictures of preterm and full-term infants using functional magnetic resonance imaging (fMRI). We also explored whether neural responses to preterm and full-term infants correlated with mothers’ self-reported tendencies to be nurturing and protective with children, and with mothers’ ratings of affection or aversion toward pictures of preterm infants. Results revealed that, compared to pictures of full-term infants, those of preterm infants elicited more activity in specific areas of the brain (dmPFC, right insula, left caudate, hippocampi, parahippocampi, and PAG), that have previously been associated with processing of negative emotions and with empathy. In addition, less activity was seen in one area of the brain (vmPFC) known to be associated with reward-motivation or mental state understanding and perspective-taking. Higher self-reported maternal nurturance was associated with increased activity to pictures of preterm infants vs full-term infants in the caudate, which might reflect approach- or reward-related processing. To conclude, neural responses to preterm infants are related to reward-motivation, mentalizing, negative emotions, and empathy. Future studies should examine whether such neural processing of preterm infant stimuli might underlie difficulties in the parent–child relationship of parents with a preterm child.

Serotonin differentially modulates the temporal dynamics of the limbic response to facial emotions in male adults with and without autism spectrum disorder (ASD): a randomised placebo-controlled single-dose crossover trial

Emotion processing—including signals from facial expressions—is often altered in individuals with autism spectrum disorder (ASD). The biological basis of this is poorly understood but may include neurochemically mediated differences in the responsivity of key ‘limbic’ regions (including amygdala, ventromedial prefrontal cortex (vmPFC) and nucleus accumbens (NAc)). Emerging evidence also suggests that ASD may be a disorder of brain temporal dynamics. Moreover, serotonin (5-HT) has been shown to be a key regulator of both facial-emotion processing and brain dynamics, and 5-HT abnormalities have been consistently implicated in ASD. To date, however, no one has examined how 5-HT influences the dynamics of facial-emotion processing in ASD. Therefore, we compared the influence of 5-HT on the responsivity of brain dynamics during facial-emotion processing in individuals with and without ASD. Participants completed a facial-emotion processing fMRI task at least 8 days apart using a randomised double-blind crossover design. At each visit they received either a single 20-mg oral dose of the selective serotonin reuptake inhibitor (SSRI) citalopram or placebo. We found that citalopram (which increases levels of 5-HT) caused sustained activation in key limbic regions during processing of negative facial emotions in adults with ASD—but not in neurotypical adults. The neurotypical adults’ limbic response reverted more rapidly to baseline following a 5-HT-challenge. Our results suggest that serotonergic homoeostatic control of the temporal dynamics in limbic regions is altered in adults with ASD, and provide a fresh perspective on the biology of ASD.

A Double Dissociation Between Anxiety and Depression Symptom Improvement and Fusiform Coupling During Positive and Negative Emotional Face Processing

A Double Dissociation Between Anxiety and Depression Symptom Improvement and Fusiform Coupling During Positive and Negative Emotional Face Processing

Brain functional effects of electroconvulsive therapy during emotional processing in major depressive disorder

BackgroundIn treatment-resistant major depressive disorder (MDD), electroconvulsive therapy (ECT) is a treatment with high efficacy. While knowledge regarding changes in brain structure following ECT is growing, the effects of ECT on brain function during emotional processing are largely unknown. ObjectiveWe investigated the effects of ECT on the activity of the anterior cingulate cortex (ACC) and amygdala during negative emotional stimuli processing and its association with clinical response. MethodsIn this non-randomized longitudinal study, patients with MDD (n = 37) were assessed before and after treatment with ECT. Healthy controls (n = 37) were matched regarding age and gender. Functional magnetic resonance imaging (fMRI) was obtained twice, at baseline and after six weeks using a supraliminal face-matching paradigm. In order to evaluate effects of clinical response, additional post-hoc analyses were performed comparing responders to non-responders. ResultsAfter ECT, patients with MDD showed a statistically significant increase in ACC activity during processing of negative emotional stimuli (pFWE = .039). This effect was driven by responders (pFWE = .023), while non-responders showed no increase. Responders also had lower pre-treatment ACC activity compared to non-responders (pFWE = .025). No significant effects in the amygdala could be observed. ConclusionsECT leads to brain functional changes in the ACC, a relevant region for emotional regulation during processing of negative stimuli. Furthermore, baseline ACC activity might serve as a biomarker for treatment response. Findings are in accordance with recent studies highlighting properties of pre-treatment ACC to be associated with general antidepressive treatment response.

Recognition of musical emotions in the behavioral variant of frontotemporal dementia

IntroductionMultiple investigations have revealed that patients with behavioral variant of frontotemporal dementia (bvFTD) experience difficulty recognizing emotional signals in multiple processing modalities (e.g., faces, prosody). Few studies have evaluated the recognition of musical emotions in these patients. This research aims to evaluate the ability of subjects with bvFTD to recognize musical stimuli with positive and negative emotions, in comparison with healthy subjects. MethodsbvFTD (n=12) and healthy control participants (n=24) underwent a test of musical emotion recognition: 56 fragments of piano music were randomly reproduced, 14 for each of the emotions (happiness, sadness, fear, and peacefulness). ResultsIn the subjects with bvFTD, a mean of correct answers of 23.6 (42.26%) was observed in contrast to the control subjects, where the average number of correct answers was 36.3 (64.8%). Statistically significant differences were found for each of the evaluated musical emotions and in the total score on the performed test (P<.01). The within-group analysis showed greater difficulty for both groups in recognizing negative musical emotions (sadness, fear), with the subjects with bvFTD exhibiting worse performance. ConclusionsOur results indicate that the recognition of musical stimuli with positive (happiness, peacefulness) and negative (sadness, fear) emotions are compromised in patients with bvFTD. The processing of negative musical emotions is the most difficult for these individuals.

Neurocognitive reorganization of emotional processing following a socio-cognitive intervention in Colombian ex-combatants

ABSTRACT Ex-combatants often exhibit atypical Emotional Processing (EP) such as reduced emphatic levels and higher aggressive attitudes. Social Cognitive Training (SCT) addressing socio-emotional components powerfully improve social interaction among Colombian ex-combatants. However, with narrow neural evidence, this study offers a new testimony. A sample of 28 ex-combatants from Colombian illegal armed groups took part in this study, split into 15 for SCT and 13 for the conventional program offered by the Governmental Reintegration Route. All of them were assessed before and after the intervention with a protocol that included an EP task synchronized with electroencephalographic recordings. We drew behavioral scores and brain connectivity (Coherency) metrics from task performance. Behavioral scores yielded no significant effects. Increased post-intervention connectivity in the delta band was observed during negative emotional processing only SCT group. Positive emotions exposed distinctive gamma band connectivity that differentiate groups. These results suggest that SCT can trigger covert neurofunctional reorganization in ex-combatants embarked on the reintegration process even when overt behavioral improvements are not yet apparent. Such covert functional changes may be the neural signature of compensatory mechanisms necessary to reshape behaviors adaptively. This novel framework may inspire cutting-edge translational research at the crossing of neuroscience, sociology, and public policy-making.

Modulation of amygdala reactivity following rapidly acting interventions for major depression.

Electroconvulsive therapy (ECT) and ketamine treatment both induce rapidly acting antidepressant effects in patients with major depressive disorder unresponsive to standard treatments, yet their specific impact on emotion processing is unknown. Here, we examined the neural underpinnings of emotion processing within and across patients (N = 44) receiving either ECT (N = 17, mean age: 36.8, 11.0 SD) or repeated subanesthetic (0.5 mg/kg) intravenous ketamine therapy (N = 27, mean age: 37.3, 10.8 SD) using a naturalistic study design. MRI and clinical data were collected before (TP1) and after treatment (TP2); healthy controls (N = 31, mean age: 34.5, 13.5 SD) completed one MRI session (TP1). An fMRI face‐matching task probed negative‐ and positive‐valence systems. Whole‐brain analysis, comparing neurofunctional changes within and across treatment groups, targeted brain regions involved in emotional facial processing, and included regions‐of‐interest analysis of amygdala responsivity. Main findings revealed a decrease in amygdalar reactivity after both ECT and ketamine for positive and negative emotional face processing (p < .05 family wise‐error (FWE) corrected). Subthreshold changes were observed between treatments within the dorsolateral prefrontal cortex and insula (p < .005, uncorrected). BOLD change for positive faces in the inferior parietal cortex significantly correlated with overall symptom improvement, and BOLD change in frontal regions correlated with anxiety for negative faces, and anhedonia for positive faces (p < .05 FWE corrected). Both serial ketamine and ECT treatment modulate amygdala response, while more subtle treatment‐specific changes occur in the larger functional network. Findings point to both common and differential mechanistic upstream systems‐level effects relating to fast‐acting antidepressant response, and symptoms of anxiety and anhedonia, for the processing of emotionally valenced stimuli.

Maternal emotion socialization in early childhood predicts adolescents' amygdala-vmPFC functional connectivity to emotion faces.

Guided by Eisenberg, Cumberland, and Spinrad's (1998) conceptual framework, we examined multiple components of maternal emotion socialization (i.e., reactions to children's negative emotion, emotion talk, emotional expressiveness) at 33 months of age as predictors of adolescents' amygdala-vmPFC connectivity and amygdala activation when labeling and passively observing angry and happy faces. For angry faces, more positive maternal emotion socialization behaviors predicted (a) less positive amygdala-vmPFC connectivity, which may reflect more mature vmPFC downregulation of the amygdala activation underlying implicit emotion regulation, and (b) more amygdala activation, which may reflect higher sensitivity to others' emotional cues. Associations between negative emotion socialization behaviors and neural responses to angry faces were nonsignificant, and findings for the models predicting neural responses to happy faces showed a less consistent pattern. By expanding Eisenberg et al.'s (1998) framework to consider neural processing of negative emotions, the current findings point toward the potential long-term implications of positive emotion socialization experiences during early childhood for optimal functioning of the amygdala-vmPFC circuitry during adolescence. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

Violent Behavior Is Associated With Emotion Salience Network Dysconnectivity in Schizophrenia.

Background: Despite individuals with schizophrenia being at an elevated risk of violence compared to the general population, limited efforts have been invested in investigating the neurobiological etiology explaining the increase. Among the few studies examining functional disruptions pertaining to violent schizophrenia patients using fMRI, only one study has considered functional connectivity. The current state of knowledge does not allow to infer deficits in functional connectivity specific to distinct cognitive/emotional states that have been associated with the emergence of violence in schizophrenia, such as negative emotion processing. This study sought to identify disrupted connectivity among men with schizophrenia and a history of violence (SCZ+V), compared to men with schizophrenia without a history of violence (SCZ-V) and healthy controls, during negative emotion processing using fMRI.Methods: Twenty SCZ+V, 19 SCZ-V, and 21 healthy men were scanned while viewing negative images.Results: Negative images elicited an increased connectivity between the dorsal anterior cingulate cortex (dACC) and the bilateral rostral prefrontal cortex (rPFC), as well as a decreased functional connectivity between the frontal regions (bilateral rPFC and dACC) and the putamen and hippocampus in SCZ+V men as compared to SCZ-V men and healthy controls. Concurrently, the centrality of the dACC within the network was reduced in SCV+V subjects.Conclusions: These results suggest an inefficient integration of the information by the dACC between frontal and limbic regions in SCZ+V men during negative emotion processing and highlight the importance of the ACC in the neurobiological bases of violent behavior in schizophrenia.

Emotional recognition training modifies neural response to emotional faces but does not improve mood in healthy volunteers with high levels of depressive symptoms.

There is demand for new, effective and scalable treatments for depression, and development of new forms of cognitive bias modification (CBM) of negative emotional processing biases has been suggested as possible interventions to meet this need. We report two double blind RCTs, in which volunteers with high levels of depressive symptoms (Beck Depression Inventory ii (BDI-ii) > 14) completed a brief course of emotion recognition training (a novel form of CBM using faces) or sham training. In Study 1 (N = 36), participants completed a post-training emotion recognition task whilst undergoing functional magnetic resonance imaging to investigate neural correlates of CBM. In Study 2 (N = 190), measures of mood were assessed post-training, and at 2-week and 6-week follow-up. In both studies, CBM resulted in an initial change in emotion recognition bias, which (in Study 2) persisted for 6 weeks after the end of training. In Study 1, CBM resulted in increases neural activation to happy faces, with this effect driven by an increase in neural activity in the medial prefrontal cortex and bilateral amygdala. In Study 2, CBM did not lead to a reduction in depressive symptoms on the BDI-ii, or on related measures of mood, motivation and persistence, or depressive interpretation bias at either 2 or 6-week follow-ups. CBM of emotion recognition has effects on neural activity that are similar in some respects to those induced by Selective Serotonin Reuptake Inhibitors (SSRI) administration (Study 1), but we find no evidence that this had any later effect on self-reported mood in an analogue sample of non-clinical volunteers with low mood (Study 2).

Modeling the relationship between attachment styles and somatic symptoms with the mediating role of emotional processing.

INTRODUCTION:In spite of our general knowledge about psychological roots and defects of developmental processes in the formation of somatic symptoms, the effect of the interaction of developmental components with cognitive-emotional variables is unclear. Previous researches suggest that individuals with insecure attachment may have a higher risk to experience of somatic symptoms. The main aim of this study is “Modeling the Relationship between Attachment Styles and Somatic Symptoms with the Mediating Role of Emotional Processing.”MATERIALS AND METHODS:This study was a descriptive-correlational study. Two hundred and twenty individuals aged 18–59 years living in Tehran were selected by available sampling from the general population. Collins and Reed's Adult Attachment Scale, Baker's Emotional Processing Scale, and Patient Health Questionnaire were used to collecting data. Data analysis was performed by Pearson correlation and independent t-test. The conceptual model presented in this study was tested with a path analysis approach.RESULTS:Given the Chi-squared size (χ2= 1.214; P > 0.05), it can be said that the proposed conceptual model fits well with the observed model. Besides, checking the other absolute and relative indices also shows a very good fit of the model.CONCLUSION:Our results showed that when the reciprocal effects of attachment styles were controlled, secure attachment could be considered as a protective factor against deficits in emotional processing and somatization of negative emotions. On the other hand, we found that when the dominant attachment style in individuals was anxiety based, it could be possible that they experience deficiency in the processing of emotion and more severe somatic symptoms.

Associations between Facial Emotion Recognition and Mental Health in Early Adolescence.

Research shows that adolescents with mental illnesses have a bias for processing negative facial emotions, and this may play a role in impaired social functioning that often co-exists with a mental health diagnosis. This study examined associations between psychological and somatic problems and facial emotion recognition in early adolescence; as any processing biases in this age-group may be an early indicator of later mental illnesses. A community sample of 40 12-year-olds self-rated their symptoms of anxiety, depression, and somatization via two mental health screeners. They also completed a computerized emotion recognition task in which they identified photographs of 40 faces showing expressions of anger, fear, sadness, happiness, or neutral expression. Results showed that increased symptoms of anxiety, depression, and somatization were significantly associated with fewer correct responses to angry expressions. These symptoms were also associated with faster and more accurate recognition of fearful expressions. However, there was no association between mental health and recognition of sad affect. Finally, increased psychological and/or somatic symptomology was also associated with better identification of neutral expressions. In conclusion, youth with increased psychological and/or somatic problems exhibited a processing bias for negative anger and fear expressions, but not sadness. They showed better processing of neutral faces than youth with fewer psychological and/or somatic problems. Findings are discussed in relation to indicators of mental illnesses in early adolescence and the potential underpinning neural mechanisms associated with mental health and emotional facial recognition.

Presentation of familiar odor induces negative dream emotions during rapid eye movement (REM) sleep in healthy adolescents

ObjectiveOdor presentation is a crucial tool in the experimental investigation of dreaming since odors rarely cause arousal, and are processed in the brain during sleep. Our previous study demonstrated that the presentation of a preferred odor during rapid eye movement (REM) sleep-induced negative dream emotions. However, preference and familiarity of an odor are known to be strongly related to each other in olfactory perception. Consequently, the above result might have been due to the confounding effects of familiarity. Therefore, the present study was designed to clarify the effects of an individual's degree of familiarity with an odor on negative emotions experienced when dreaming. MethodsThe airflow with phenylethyl alcohol (PEA: rose-like smell) was presented as a stimulus of experimental condition, and odorless airflow was presented as the control. Participants who were familiar (n = 7) and unfamiliar (n = 7) with the odor of PEA experienced both conditions during REM sleep in the second and later sleep cycle. Then, they were awakened, and they rated the characteristics of their dream using a questionnaire. Results and conclusionsParticipants who were familiar with the odor of PEA rated their dreams more negatively in the experimental condition relative to the control condition. It is concluded based on these results that a familiar odor may induce negative emotion in dreams, possibly because familiar odors tend to be perceived more strongly, and the olfactory pathway has direct connections to the amygdala, which is primarily involved in processing negative emotions.

Fear conditioning and extinction in alcohol dependence: Evidence for abnormal amygdala reactivity.

Fear conditioning and extinction (FCE) are vital processes in adaptive emotion regulation and disrupted in anxiety disorders. Despite substantial comorbidity between alcohol dependence (ALC) and anxiety disorders and reports of altered negative emotion processing in ALC, neural correlates of FCE in this clinical population remain unknown. Here, we used a 2-day fear learning paradigm in 43 healthy participants and 43 individuals with ALC at the National Institutes of Health. Main outcomes of this multimodal study included structural and functional brain magnetic resonance imaging, clinical measures, as well as skin conductance responses (SCRs) to confirm differential conditioning. Successful FCE was demonstrated across participants by differential SCRs in the conditioning phase and no difference in SCRs to the conditioned stimuli in the extinction phase. The ALC group showed significantly reduced blood oxygenation level-dependent responses in the right amygdala during conditioning (Cohen's d = .89, P(FWE) = .037) and in the left amygdala during fear renewal (Cohen's d = .68, P(FWE) = .039). Right amygdala activation during conditioning was significantly correlated with ALC severity (r = .39, P(Bonferroni) = .009), depressive symptoms (r = .37, P(Bonferroni) = .015), trait anxiety (r = .41, P(Bonferroni) = .006), and perceived stress (r = .45, P(Bonferroni) = .002). Our data suggest that individuals with ALC have dysregulated fear learning, in particular, dysregulated neural activation patterns, in the amygdala. Furthermore, amygdala activation during fear conditioning was associated with ALC-related clinical measures. The FCE paradigm may be a promising tool to investigate structures involved in negative affect regulation, which might inform the development of novel treatment approaches for ALC.

Affective factors explaining the association between depressive functioning and alcohol outcomes among college students

Rates of co-occurring depression and alcohol use are higher among college students than in the general population. Further research is needed to illuminate how the mechanisms with which individuals process negative emotions may clarify the link between depressive symptoms and drinking. Objective: To assess how three potential mediators representing affective functioning (ie, need for affect, distress tolerance, emotion regulation) explain the relationship between depressive symptoms and alcohol use (ie, quantity and problems). Participants: The sample consisted of 227 college student heavy drinkers. Methods: Participants completed computerized self-report surveys in Fall 2016. Results: Path analyses revealed need for affect mediated the association between depressive symptoms and alcohol quantity, while emotion regulation mediated the relationship between depressive symptoms and alcohol-related problems. Conclusions: Findings highlight the importance of various affective functioning mechanisms to the depressive symptom-drinking link. Future research could target these mechanisms in college interventions for co-occurring mood symptoms and alcohol use.

Effects of Expressive Writing on Neural Processing During Learning.

Expressive writing about past negative events has been shown to lead to a slew of positive outcomes. However, little is known about why writing about something negative would have positive effects. While some have posited that telling a narrative of a past negative event or current anxiety “frees up” cognitive resources, allowing individuals to focus more on the task at hand, there is little neural evidence suggesting that expressive writing has an effect on cognitive load. Moreover, little is known about how individual differences in the content of expressive writing could affect neural processing and the cognitive benefits writing confers. In our experiment, we compared brain activity in a group that had engaged in expressive writing vs. a control group, during performance on a feedback-based paired-associate word-learning task. We found that across groups, differential activation in the dorsal striatum in response to positive vs. negative feedback significantly predicted better later memory. Moreover, writing about a past failure resulted in more activation relative to the control group during the learning task in the mid-cingulate cortex (MCC), an area of the brain crucial to processing negative emotion. While our results do not provide support for the assertion that expressive writing alters attentional processing, our findings suggest that choosing to write about particularly intense past negative experiences like a difficult past failure may have resulted in changes in neural activation during task processing.

Brain Functional Basis of Subjective Well-being During Negative Facial Emotion Processing Task-Based fMRI

Subjective well-being (SWB) is the eternal pursuit of all mankind. Individual differences in SWB may reflect the way of emotional processing. Neuroimaging studies have partly examined the neural mechanism of the individual differences in SWB using resting-state functional magnetic resonance imaging (rs-fMRI). However, few studies have investigated the relationship between the individual differences in SWB and brain functional connectivity during facial emotion processing task. Here, we applied negative facial emotion processing task-based fMRI to explore the brain functional basis of the individual differences in SWB. Results showed that SWB is positively correlated with the activation of right posterior cingulate cortex, left interior temporal gyrus and left angular gyrus for the comparison of negative stimulus and neutral stimulus, revealing that happy individuals may be more proactive to use attention transfer and behavioral inhibition strategies to decrease negative experiences during negative emotional processing. In addition, high SWB is associated with strong functional connectivity between high-level cognitive networks (e.g., frontal-parietal network) and low-level perceptual networks (e.g., sensorimotor network), and weak functional connectivity within default mode network and within low-level perceptual networks, indicating that the self-reflection, emotional regulation and cognitive control during negative facial emotion processing underlies the individual differences in SWB. These findings provide a novel insight to characterize the brain functional basis of the individual differences in SWB.

Negative emotional state slows down movement speed: behavioral and neural evidence.

BackgroundAthletic performance is affected by emotional state. Athletes may underperform in competition due to poor emotion regulation. Movement speed plays an important role in many competition events. Flexible control of movement speed is critical for effective athletic performance. Although behavioral evidence showed that negative emotion can influence movement speed, the nature of the relationship remains controversial. Thus, the present study investigated how negative emotion affects movement speed and the neural mechanism underlying the interaction between emotion processing and movement control.MethodsThe present study combined electroencephalography (EEG) technology with a cued-action task to investigate the effect of negative emotion on movement speed. In total, 21 undergraduate students were recruited for this study. Participants were asked to perform six consecutive action tasks after viewing an emotional picture. Pictures were presented in two blocks (one negative and one neutral). After the participants completed a set of tasks (neutral of negative), they were subjected to complete a 9-point self-assessment manikin scale. Participants underwent EEG while performing the tasks.ResultsAt the behavior level, there was a significant main effect of emotional valence on movement speed, with participants exhibiting significantly slower movements in the negative emotional condition than in the neutral condition. EEG data showed increased theta oscillation and larger P1 amplitude in response to negative than to neural images suggesting that more cognitive resources were required to process negative than neutral images. EEG data also showed a larger late CNV area in the neutral condition than in the negative condition, which suggested that there was a significant decrease in brain activation during action tasks in negative emotional condition than in the neural. While the early CNV did not reveal a significant main effect of emotional valence.ConclusionThe present results indicate that a negative emotion can slow movement, which is largely due to negative emotional processing consuming more resources than non-emotional processing and this interference effect mainly occurred in the late movement preparation phase.

PACAP regulation of central amygdala GABAergic synapses is altered by restraint stress

The pituitary adenylate cyclase-activating polypeptide (PACAP) system plays a central role in the brain's emotional response to psychological stress by activating cellular processes and circuits associated with threat exposure. The neuropeptide PACAP and its main receptor PAC1 are expressed in the rodent central amygdala (CeA), a brain region critical in negative emotional processing, and CeA PACAPergic signaling drives anxiogenic and stress coping behaviors. Despite this behavioral evidence, PACAP's effects on neuronal activity within the medial subdivision of the CeA (CeM, the major output nucleus for the entire amygdala complex) during basal conditions and after psychological stress remain unknown. Therefore, in the present study, male Wistar rats were subjected to either restraint stress or control conditions, and PACAPergic regulation of CeM cellular function was assessed using immunohistochemistry and whole-cell patch-clamp electrophysiology. Our results demonstrate that PACAP-38 potentiates GABA release in the CeM of naïve rats, via its actions at presynaptic PAC1. Basal PAC1 activity also enhances GABA release in an action potential-dependent manner. Notably, PACAP-38's facilitation of CeM GABA release was attenuated after a single restraint stress session, but after repeated sessions returned to the level observed in naïve animals. A single restraint session also significantly decreased PAC1 levels in the CeM, with repeated restraint sessions producing a slight recovery. Collectively our data reveal that PACAP/PAC1 signaling enhances inhibitory control of the CeM and that psychological stress can modulate this influence to potentially disinhibit downstream effector regions that mediate anxiety and stress-related behaviors.This article is part of the special issue on ‘Neuropeptides’.

Gamma-Aminobutyric Acid Levels in the Anterior Cingulate Cortex of Perimenopausal Women With Depression: A Magnetic Resonance Spectroscopy Study.

ObjectiveThe anterior cingulate cortex (ACC) is associated with the processing of negative emotions. Gamma-aminobutyric acid (GABA) metabolism plays an important role in the pathogenesis of mental disorders. We aimed to determine the changes in GABA levels in the ACC of perimenopausal women with depression.MethodsWe recruited 120 perimenopausal women, who were followed up for 18–24 months. After reaching menopause, the participants were divided into a control group (n = 71), an anxiety group (n = 30), and a depression group (n = 19). The participants were examined using proton magnetic resonance spectroscopy (MRS). TARQUIN software was used to calculate the GABA concentrations in the ACC before and after menopause. The relationship of the GABA levels with the patients’ scores on the 14-item Hamilton Anxiety Scale and 17-item Hamilton Depression Scale was determined.ResultsGABA decreased with time. The postmenopausal GABA levels were significantly lower in the depression group than in the anxiety group and were significantly lower in both these groups than in the normal group. The postmenopausal GABA levels were significantly lower than the premenopausal levels in the normal, anxiety, and depression groups (P = 0.014, <0.001, and <0.001, respectively). The premenopausal GABA levels did not significantly differ between the normal vs. anxiety group (P = 0.907), normal vs. depression group (P = 0.495), and anxiety vs. depression group. The postmenopausal GABA levels were significantly lower in the depression group than in the anxiety group and were significantly lower in both these groups than in the normal group, normal vs. anxiety group (P = 0.022), normal vs. depression group (P < 0.001), and anxiety vs. depression group (P = 0.047).ConclusionChanges in GABA concentrations in the anterior cingulate cortex are related with the pathophysiological mechanism and symptoms of perimenopausal depression.