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We examined the long-term causal effects of an evidence-based parenting program delivered in infancy on children’s emotion regulation and resting-state functional connectivity (rs-fc) during middle childhood. Families were referred to the study by Child Protective Services (CPS) as part of a diversion from a foster care program. A low-risk group of families was also recruited. CPS-involved families were randomly assigned to receive the target (Attachment and Biobehavioral Catch-up, ABC) or a control intervention (Developmental Education for Families, DEF) before infants turned 2. Both interventions were home-based, manualized, and 10-sessions long. During middle childhood, children underwent a 6-min resting-state functional MRI scan. Amygdala seed-based rs-fc analysis was completed with intervention group as the group-level predictor of interest. Fifty-seven children ( N ABC = 21; N DEF = 17; N COMP = 19; M age = 10.02 years, range = 8.08–12.14) were scanned successfully. The DEF group evidenced negative left amygdala↔OFC connectivity, whereas connectivity was near zero in the ABC and comparison groups (ABCvsDEF: Cohen’s d = 1.17). ABC may enhance high-risk children’s regulatory neurobiology outcomes ∼8 years after the intervention was completed.

Die geringe Kontrollierbarkeit repetitiver Schmerzattacken ist eine der bedeutendsten Ursachen für die eingeschränkte Lebensqualität chronischer Schmerzpatienten. Der Effekt des Kontrollerlebens auf den subjektiven Schmerz, sowie die zugrundeliegenden neuronalen Mechanismen, sind bei Schmerzpatienten noch nicht umfänglich bekannt und wurden bislang hauptsächlich bei gesunden Kontrollprobanden untersucht. In diesem Vortrag soll die neuronale Modulation experimenteller Schmerzreize durch Kontrollerleben bei Patientinnen mit Fibromyalgie (FM) und gesunden Probandinnen vorgestellt werden. Mittels funktioneller Magnetresonanztomographie (fMRT) wurden die neuronalen Korrelate selbst zu beendender Hitzereize mit physikalisch in Intensität und Dauer identischen, jedoch external kontrollierten Hitzereizen, verglichen. Im Gegensatz zur Kontrollgruppe, konnten die Patientinnen mit FM nicht die in die Schmerzmodulation involvierten Hirnregionen, wie den rechten ventrolateralen prefrontal Cortex (VLPFC), den dorsolateralen prefrontal Cortex (DLPFC) und den dorsalen anterioren cingulären Cortex (dACC), aktivierten. Extern kontrollierte Hitzereize aktivierten bei der Kontrollgruppe den orbitofrontalen Cortex, während die Patientinnen mit FM Strukturen, die in die Emotionsverarbeitung involviert sind (Amygdala, parahippocampal Gyrus), aktivierten. Weiterhin zeigten Patientinnen mit FM bei selbstkontrollierten Hitzereizen eine gestörte funktionelle Konnektivität des VLPFC, DLPFC und dACC mit somatosensorischen und schmerzinhibitorischen Arealen. Außerdem wurde ein reduziertes Volumen der grauen Substanz im DLPFC und dACC bei FM gefunden. Die beschriebenen funktionellen und strukturellen Veränderungen weisen auf eine dysfunktionale neuronale Schmerzmodulation durch erlebte Kontrolle bei FM hin. Diese extensiven funktionellen und strukturellen Veränderungen in relevanten sensorischen, limbischen und assoziativen Hirnarealen könnten über Behandlungen wie TMS, Neurofeedback oder Verhaltenstrainings adressiert werden.

The mechanisms linking ovarian hormones to negative affect are poorly characterized, but important clues may come from the examination of the brain's intrinsic organization. Here, we studied the effects of both the menstrual cycle and oral contraceptives (OCs) on amygdala and salience network resting-state functional connectivity using a double-blind, randomized, and placebo-controlled design. Hormone levels, depressive symptoms, and resting-state functional connectivity were measured in 35 healthy women (24.9±4.2 years) who had previously experienced OC-related negative affect. All participants were examined in the follicular phase of a baseline cycle and in the third week of the subsequent cycle during treatment with either a combined OC (30 μg ethinyl estradiol/0.15 mg levonorgestrel) or placebo. The latter time point targeted the midluteal phase in placebo users and steady-state ethinyl estradiol and levonorgestrel concentrations in OC users. Amygdala and salience network connectivity generally increased with both higher endogenous and synthetic hormone levels, although amygdala-parietal cortical connectivity decreased in OC users. When in the luteal phase, the naturally cycling placebo users demonstrated higher connectivity in both networks compared with the women receiving OCs. Our results support a causal link between the exogenous administration of synthetic hormones and amygdala and salience network connectivity. Furthermore, they suggest a similar, potentially stronger, association between the natural hormonal variations across the menstrual cycle and intrinsic network connectivity.

Depression is associated with systemic inflammation, and the systemic inflammation caused by endotoxin administration elicits mild depressive symptoms such as fatigue and reduced interest. The neural correlates of depressive symptoms that result from systemic inflammation are poorly defined. The aim of this study was to use (18)F-FDG PET to identify brain regions involved in the response to endotoxin administration in humans. Nine healthy subjects received double-blind endotoxin (0.8 ng/kg) and placebo on different days. (18)F-FDG PET was used to measure differences in the cerebral metabolic rate of glucose in the following regions of interest: insula, cingulate, and amygdala. Serum levels of tumor necrosis factor-α and interleukin-6 were used to gauge the systemic inflammatory response, and depressive symptoms were measured with the Montgomery-Åsberg Depression Rating Scale and other scales. Endotoxin administration was associated with an increase in Montgomery-Åsberg Depression Rating Scale, increased fatigue, reduced social interest, increased levels of inflammatory cytokines, higher normalized glucose metabolism (NGM) in the insula, and, at a trend level, lower NGM in the cingulate. Secondary analyses of insula and cingulate subregions indicated that these changes were driven by the right anterior insula and the right anterior cingulate. There was a negative correlation between peak cytokine levels and change in social interest and between peak cytokine levels and change in insula NGM. There was a positive correlation between the change in NGM in the insula and change in social interest. Systemic inflammation in humans causes an increase in depressive symptoms and concurrent changes in glucose metabolism in the insula and cingulate-brain regions that are involved in interoception, positive emotionality, and motivation.

Stress is assumed to cause a shift from flexible 'cognitive' memory to more rigid 'habit' memory. In the spatial memory domain, stress impairs place learning depending on the hippocampus whereas stimulus-response learning based on the striatum appears to be improved. While the neural basis of this shift is still unclear, previous evidence in rodents points towards cortisol interacting with the mineralocorticoid receptor (MR) to affect amygdala functioning. The amygdala is in turn assumed to orchestrate the stress-induced shift in memory processing. However, an integrative study testing these mechanisms in humans is lacking. Therefore, we combined functional neuroimaging of a spatial memory task, stress-induction, and administration of an MR-antagonist in a full-factorial, randomized, placebo-controlled between-subjects design in 101 healthy males. We demonstrate that stress-induced increases in cortisol lead to enhanced stimulus-response learning, accompanied by increased amygdala activity and connectivity to the striatum. Importantly, this shift was prevented by an acute administration of the MR-antagonist spironolactone. Our findings support a model in which the MR and the amygdala play an important role in the stress-induced shift towards habit memory systems, revealing a fundamental mechanism of adaptively allocating neural resources that may have implications for stress-related mental disorders.

Meditation training can improve mood and emotion regulation, yet the neural mechanisms of these affective changes have yet to be fully elucidated. We evaluated the impact of long- and short-term mindfulness meditation training on the amygdala response to emotional pictures in a healthy, non-clinical population of adults using blood-oxygen level dependent functional magnetic resonance imaging. Long-term meditators (N = 30, 16 female) had 9081 h of lifetime practice on average, primarily in mindfulness meditation. Short-term training consisted of an 8-week Mindfulness- Based Stress Reduction course (N = 32, 22 female), which was compared to an active control condition (N = 35, 19 female) in a randomized controlled trial. Meditation training was associated with less amygdala reactivity to positive pictures relative to controls, but there were no group differences in response to negative pictures. Reductions in reactivity to negative stimuli may require more practice experience or concentrated practice, as hours of retreat practice in long-term meditators was associated with lower amygdala reactivity to negative pictures – yet we did not see this relationship for practice time with MBSR. Short-term training, compared to the control intervention, also led to increased functional connectivity between the amygdala and a region implicated in emotion regulation – ventromedial prefrontal cortex (VMPFC) – during affective pictures. Thus, meditation training may improve affective responding through reduced amygdala reactivity, and heightened amygdala–VMPFC connectivity during affective stimuli may reflect a potential mechanism by which MBSR exerts salutary effects on emotion regulation ability. •Mindfulness meditation related to lower amygdala activation to positive pictures.•Amygdala-prefrontal coupling increased after Mindfulness-Based Stress Reduction.•Amygdala activation to negative pictures was lower with more practice on retreat.

Abstract Lower neighborhood socioeconomic status (nSES) is associated with poorer cognitive function; underlying neural correlates are unknown. Cross-sectional associations of nSES (six census-derived measures of income, education, and occupation) and gray matter volume (GMV) of eight memory-related regions (hippocampus, middle frontal gyrus, amygdala, insula, parahippocampal gyrus, anterior, middle, and posterior cingulum) were examined in 264 community-dwelling older adults (mean age=83, 56.82% female, 39.02% black). In linear mixed effects models adjusted for total brain atrophy and accounting for geographic clustering, higher nSES was associated with greater GMV of the left hippocampus, left posterior cingulum, and bilateral insula, middle frontal, and parahippocampal gyri. nSES remained associated with GMV of the right insula (β= -32.26, p=0.026, 95%CI: -60.66, -3.86) after adjusting for individual level age, gender, race, income, and education. The nSES and cognitive function association may not be due to gray matter volume differences; other behavioral and biological mediators should be explored.

We interact socially and form bonds with others because such experiences are rewarding. However, an insecure attachment style or social anxiety can reduce these rewarding effects. The neuropeptide oxytocin (OXT) may facilitate social interactions either by increasing their rewarding experience or by attenuating anxiety, although effects can be sex- and attachment-style dependent. In this study, 128 pairs of same-sex friends completed a social sharing paradigm in a double-blind, placebo-controlled, between-subject design with one friend inside an MRI scanner and the other in a remote behavioral testing room. In this way we could examine whether intranasal-OXT differentially modulated the emotional impact of social sharing and associated neural processing. Additionally, we investigated if OXT effects were modulated by sex and attachment style. Results showed that in women, but not men, OXT increased ratings for sharing stimuli with their friend but not with a stranger, particularly in the friend in the scanner. Corresponding neuroimaging results showed that OXT decreased both amygdala and insula activity as well as their functional connectivity in women when they shared with friends but had the opposite effect in men. On the other hand, OXT did not enhance responses in brain reward circuitry. In the PLC treated group amygdala responses in women when they shared pictures with their friend were positively associated with attachment anxiety and OXT uncoupled this. Our findings demonstrate that OXT facilitates the impact of sharing positive experiences with others in women, but not men, and that this is associated with differential effects on the amygdala and insula and their functional connections. Furthermore, OXT particularly reduced increased amygdala responses during sharing in individuals with higher attachment anxiety. Thus, OXT effects in this context may be due more to reduced anxiety when sharing with a friend than to enhanced social reward. •Oxytocin facilitates social interaction by increasing reward or attenuating anxiety.•Effects may depend on sex and attachment style.•Effects of oxytocin on social sharing were assessed in 128 pairs of friends.•Oxytocin increased sharing effect and reduced amygdala/insula activity in women.•Oxytocin facilitates the impact of social sharing only in women but not men.

Preclinical evidence suggests that diazepam enhances hippocampal γ-aminobutyric acid (GABA) signalling and normalises a psychosis-relevant cortico-limbic-striatal circuit. Hippocampal network dysconnectivity, particularly from the CA1 subfield, is evident in people at clinical high-risk for psychosis (CHR-P), representing a potential treatment target. This study aimed to forward-translate this preclinical evidence. In this randomised, double-blind, placebo-controlled study, 18 CHR-P individuals underwent resting-state functional magnetic resonance imaging twice, once following a 5 mg dose of diazepam and once following a placebo. They were compared to 20 healthy controls (HC) who did not receive diazepam/placebo. Functional connectivity (FC) between the hippocampal CA1 subfield and the nucleus accumbens (NAc), amygdala, and ventromedial prefrontal cortex (vmPFC) was calculated. Mixed-effects models investigated the effect of group (CHR-P placebo/diazepam vs. HC) and condition (CHR-P diazepam vs. placebo) on CA1-to-region FC. In the placebo condition, CHR-P individuals showed significantly lower CA1-vmPFC (  = 3.17,  = 0.002) and CA1-NAc (  = 2.94,  = 0.005) FC compared to HC. In the diazepam condition, CA1-vmPFC FC was significantly increased (  = 4.13,  = 0.008) compared to placebo in CHR-P individuals, and both CA1-vmPFC and CA1-NAc FC were normalised to HC levels. In contrast, compared to HC, CA1-amygdala FC was significantly lower contralaterally and higher ipsilaterally in CHR-P individuals in both the placebo and diazepam conditions (lower: placebo  = 3.46,  = 0.002, diazepam  = 3.33,  = 0.003; higher: placebo  = 4.48,  < 0.001, diazepam  = 4.22,  < 0.001). This study demonstrates that diazepam can partially restore hippocampal CA1 dysconnectivity in CHR-P individuals, suggesting that modulation of GABAergic function might be useful in the treatment of this clinical group.