Dysfunctional decision-making in binge-eating disorder: A meta-analysis and systematic review.

Binge-Eating Disorder (BED) involves anticipatory craving and urges, subjective loss-of-control during binge-eating episodes, and post-feeding psychological distress and guilt. Evidence indicates neurocognitive dysfunctions contribute to BED onset, maintenance, and treatment response. However, an integrated understanding of how cognitive processes underpin BED symptomology is lacking. We utilised a multi-stage decision-making model defining ten cognitive processes underpinning Preference Formation, Choice Implementation, Feedback Processing, and Flexibility/Shifting, to comprehensively review research published since 2013. We used preregistered PICOS criteria to assess 1966 articles identified from PubMed, PsycInfo, and Scopus database searches. This yielded 50 studies reporting behavioural cognitive tasks outcomes, comparing individuals with BED to controls with normal and higher weight. Meta-analyses revealed a unique profile of cognitive dysfunctions that spanned all decision-making stages. Significant deficits were evident in Uncertainty Evaluation, Attentional Inhibition, Choice Consistency, and Cognitive Flexibility/Set-shifting. We propose a novel model of dysfunctional decision-making processes in BED and describe their role in binge-eating behaviour. We further highlight the potential for cognitive interventions to target these processes and address the significant treatment gap in BED.

Gender moderates the association between chronic academic stress with top-down and bottom-up attention.

Research on the relationship between chronic stress and cognition is limited by a lack of concurrent measurement of state-anxiety, physiological arousal, and gender. For the first time, we assessed the impact of these factors on top-down/conscious (simple and choice reaction time) and bottom-up/reflexive (saccadic reaction time) measures of attention using CONVIRT virtual-reality cognitive tests. Participants (N = 163) completed measures of academic stress (effort-reward imbalance; ERI) and state-anxiety while heart-rate variability was recorded continuously throughout the experiment. Gender moderated the association between academic stress with the top-down measures (b = -0.002, t = -2.023, p = .045; b = -0.063, t = -3.080, p = .002) and higher academic stress was associated with poorer/slower reaction times only for male participants. For bottom-up attention, heart rate variability moderated the relationship between academic stress and saccadic reaction time (b = 0.092, t = 1.991, p = .048), and only female participants who were more stressed (i.e., ERI ≥ 1) and displayed stronger sympathetic dominance had slower reaction times. Our findings align with emerging evidence that chronic stress is related to hyperarousal in women and cognitive decrements in men. Our findings suggest that higher ERI and sympathetic dominance during cognitive testing was associated with poorer bottom-up attention in women, whereas for men, academic stress was related with poorer top-down attention irrespective of sympathovagal balance.

Involvement of dorsal raphe nucleus serotonergic systems in social approach-avoidance behaviour and in the response to fluoxetine treatment in peri-adolescent female BALB/c mice.

Serotonergic systems are involved in the development and regulation of social behaviour, and drugs that target serotonin neurotransmission, such as selective serotonin reuptake inhibitors (SSRIs), also alter aspects of social approach-avoidance. The midbrain dorsal raphe nucleus (DR), which is a major serotonergic nucleus and main source of serotonergic innervation of the forebrain, has been proposed as an important target for SSRIs, although evidence in females is lacking. In this study, we examined the involvement of the DR serotonergic systems in social behaviour and in response to SSRI treatment, using peri-adolescent female BALB/c mice. Mice were exposed to the SSRI fluoxetine either chronically (18 mg/kg/day, in drinking water, for 12 days) or acutely (18 mg/kg, i.p.), or to vehicle control condition (0.9 % saline, i.p.), prior to being exposed to the three-chambered sociability test. Activation of serotonergic neurons across subregions of the DR were subsequently measured, using dual-label immunohistochemistry for TPH2 and c-Fos. Acute fluoxetine administration increased generalised and social avoidance, while mice exposed to chronic fluoxetine treatment showed levels of social approach behaviour that were comparable to controls. Serotonergic populations across the DR showed reduced activity following acute fluoxetine treatment. Further, activation of serotonergic neurons in the ventral DR correlated with social approach behaviour in vehicle-treated control mice. These data provide some support for the involvement of discrete populations of DR serotonergic neurons in the regulation of social approach-avoidance, although more research is needed to understand the effects and mechanisms of chronic SSRI treatment in females.

Assessing the utility of a virtual-reality neuropsychological test battery, 'CONVIRT', in detecting alcohol-induced cognitive impairment.

New technologies such as virtual reality (VR) and eye-tracking software have paved the way for more sophisticated and ecologically valid measures of cognitive function. Testing the sensitivity and reliability of such measurements in response to acute alcohol intoxication provides a first step in establishing how these measures may operate in relation to cognitive impairments observed post-concussion. Healthy young adults (N = 54, M = 20.65, SD = 2.06, 30 females) completed the CONVIRT test battery (manual simple and choice reaction-time and saccade reaction-time) at three breath alcohol concentration (BrAC) levels: 0.00%T1, 0.05%T2, 0.08%T3. Participants consumed alcoholic beverages at 30-min intervals, with BrAC monitored at 15-min intervals using a breathalyser. All three CONVIRT measures were sensitive to changes in cognitive performance induced by alcohol at BrAC levels at or exceeding 0.05%. A composite measure was also sensitive to alcohol intoxication (Cohen's d = .85 at BrAC = 0.05%; d = 1.20 at BrAC = 0.08%). Strong test-retest reliability was observed (all r < .80), with no gender differences noted. CONVIRT measures were reliable and detected dose-dependent changes in alcohol-induced cognitive impairment. Potentially, the ecologically valid measures may assist in better quantifying the effects of conditions such as concussion, on cognitive performance.

The galanin receptor-3 antagonist, SNAP 37889, inhibits cue-induced reinstatement of alcohol-seeking and increases c-Fos expression in the nucleus accumbens shell of alcohol-preferring rats.

INTRODUCTION: This study aimed to investigate the effects of the galanin-3 receptor antagonist, SNAP 37889, on c-Fos protein expression after cue-induced reinstatement of alcohol-seeking in the brains of alcohol-preferring rats. METHODS: Eighteen alcohol-preferring rats were trained to self-administer 10% v/v ethanol in the presence of response-contingent cues, which was followed by extinction. Rats were then treated with SNAP 37889 (30 mg/kg, i.p.) or vehicle, before being tested for cue-induced reinstatement. Administration of SNAP 37889 reduced cue-induced reinstatement of ethanol-seeking behaviour. To examine the effect of SNAP 37889 and cue-induced reinstatement on neuronal activation, c-Fos expression was measured in subregions of the medial prefrontal cortex and nucleus accumbens. RESULTS: SNAP 37889 administration increased c-Fos immunoreactivity in the nucleus accumbens shell, but was without effect in the nucleus accumbens core and the medial prefrontal cortex. Dual-label Fos/tyrosine hydroxylase immunohistochemistry was used to examine the effects of SNAP 37889 on dopamine neurons in the ventral tegmental area; however, no differences between SNAP 37889 and vehicle-treated rats were found. CONCLUSIONS: These data support previous findings of galanin-3 receptor involvement in cue-induced reinstatement of alcohol-seeking behaviour, and provide novel evidence that the ability of galanin-3 receptor antagonism to attenuate cue-induced reinstatement relates to activation of the nucleus accumbens shell.