BackgroundBinge consumption of alcohol is a major societal problem associated with important cognitive, physiological and neurotoxic consequences. Converging evidence highlights the need to assess binge drinking (BD) and its effects on the developing brain while taking into account gender differences. Here, we compared the brain volumetric differences between genders in college-aged binge drinkers and healthy volunteers.MethodT1-weighted magnetic resonance imaging (MRI) images of 30 binge drinkers (18 males) and 46 matched healthy volunteers (23 males) were examined using voxel-based morphometry. The anatomical scans were covaried with Alcohol Use Disorders Identification Test (AUDIT) scores. Whole brain voxel-wise group comparisons were performed using a cluster extent threshold correction.ResultsSeveral large clusters qualified with group-by-gender interactions were observed in prefrontal, striatal and medial temporal areas, whereby BD females had more volume than non-BD females, while males showed the inverse pattern of decreased volume in BD males and increased volume in non-BD males. AUDIT scores negatively correlated with volume in the right superior frontal cortex and precentral gyrus.ConclusionsThese findings dovetail with previous studies reporting that a state effect of BD in college-aged drinkers and the severity of alcohol use are associated with volumetric alterations in the cortical and subcortical areas of the brain. Our study indicates that these widespread volumetric changes vary differentially by gender, suggesting either sexual dimorphic endophenotypic risk factors, or differential neurotoxic sensitivities for males and females.

BackgroundCompulsive sexual behaviors (CSB) are relatively common and associated with significant personal and social dysfunction. The underlying neurobiology is still poorly understood. The present study examines brain volumes and resting state functional connectivity in CSB compared with matched healthy volunteers (HV).MethodsStructural MRI (MPRAGE) data were collected in 92 subjects (23 CSB males and 69 age‐matched male HV) and analyzed using voxel‐based morphometry. Resting state functional MRI data using multi‐echo planar sequence and independent components analysis (ME‐ICA) were collected in 68 subjects (23 CSB subjects and 45 age‐matched HV).ResultsCSB subjects showed greater left amygdala gray matter volumes (small volume corrected, Bonferroni adjusted P < 0.01) and reduced resting state functional connectivity between the left amygdala seed and bilateral dorsolateral prefrontal cortex (whole brain, cluster corrected FWE P < 0.05) compared with HV.ConclusionsCSB is associated with elevated volumes in limbic regions relevant to motivational salience and emotion processing, and impaired functional connectivity between prefrontal control regulatory and limbic regions. Future studies should aim to assess longitudinal measures to investigate whether these findings are risk factors that predate the onset of the behaviors or are consequences of the behaviors. Hum Brain Mapp 38:1182–1190, 2017. © 2016 Wiley Periodicals, Inc.

Background The diagnosis of complex posttraumatic stress disorder (CPTSD) was included in the 11th revised edition of the International Classification of Diseases (ICD-11). CPTSD shares trauma-specific symptoms with its sibling disorder PTSD but is additionally characterized by disturbances of the individual’s self-organization (DSO). The clinical utility of the CPTSD diagnosis has yet to be thoroughly investigated. Objective The current study aimed to examine the clinical utility of the CPTSD diagnosis, considering the upcoming implementation of ICD-11 in clinical practice. Method International field studies, construct- and validity analyses leading up to the inclusion in ICD-11 are reviewed, and the diagnostic measures; International Trauma Questionnaire (ITQ) and International Trauma Interview (ITI) are presented. Also, the relationship between CPTSD and borderline personality disorder (BPD) is elaborated in an independent analysis, to clarify their differences in clinical relevance to treatment. Treatment implications for CPTSD are discussed with reference to existing guidelines and clinical needs. Results The validation of ITQ and ITI contributes to the cementation of CPTSD in further clinical practice, providing qualified assessment of the construct, with intended informative value for both clinical communication and facilitation of treatment. CPTSD is found distinguishable from both PTSD and BPD in empirical studies, while the possibility of comorbid BPD/PTSD cases being better described as CPTSD is acknowledged. Practitioners need to employ well-established methods developed for PTSD, while considering additional DSO-symptoms in treatment of CPTSD. Conclusions The inclusion of CPTSD in ICD-11 may potentially facilitate access to more tailored treatment interventions, as well as contribute to increased research focus on disorders specifically associated with stress. The clinical utility value of this additional diagnosis is expected to reveal itself further after ICD-11 is implemented in clinical practice in 2022 and onwards. Yet, CPTSD’s diagnostic inclusion gives future optimism to assessing and treating complex posttraumatic stress symptoms.

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The inhibition of K+-stimulated [3H]dopamine and [14C]acetylcholine release from preloaded rat striatal slices was used to examine the presynaptic selectivity of the putative dopamine autoreceptor agonist, B-HT 920. In the micromolar range, B-HT 920 caused a concentration-dependent inhibition of the release of both labeled neurotransmitters as evoked by 20 mM K+. The effect of B-HT 920 on both [3H]dopamine and [14C]acetylcholine release was completely blocked by (+) butaclamol but not by (-) butaclamol. Sulpiride, a selective D2 antagonist, similarly blocked the inhibitory effect of B-HT 920 on the release of both labeled neurotransmitters indicating both responses were mediated by D2 receptors. (+) Butaclamol alone elevated stimulated [3H]dopamine release suggesting a significant amount of autoreceptor occupancy by endogenously released dopamine. Experiments with tolazoline and the alpha 2 agonist, B-HT 933, did not suggest any involvement of alpha-adrenoceptor activity in the inhibitory effects of B-HT 920 on the release of either transmitter. Inhibition of release was a selective effect of B-HT 920 as the drug was without effect on the K+-stimulated release of [3H]serotonin. The results indicate that in vitro B-HT 920 is active of both pre- and postsynaptic dopamine receptors in contrast to the pattern of effects observed after its in vivo administration.

Natural rewards such as erotic stimuli activate common neural pathways with monetary rewards. In human studies, the manipulation of dopamine and serotonin play an important role in the processing of monetary rewards with less understood on its role on erotic stimuli. In this study, we investigate the neuromodulatory effects of dopaminergic and serotonergic transmission in the processing of erotic versus monetary visual stimuli. We scanned one hundred and two (N = 102) healthy volunteers using functional magnetic resonance imaging while performing a modified version of the well-validated monetary incentive delay task consisting of erotic, monetary and neutral visual stimuli. We show a role for enhanced central dopamine and lowered central serotonin levels in increasing activity in the right caudate and left anterior insula during anticipation of erotic relative to monetary rewards in healthy controls. We further show differential activation in the anticipation of natural versus monetary rewards with the former associated with ventromesial and dorsomesial activity and the latter with dorsal cingulate, striatal and anterior insular activity. These findings are consistent with preclinical and clinical findings of a role for dopaminergic and serotonergic mechanisms in the processing of natural rewards. Our study provides further insights into the neural substrates underlying reward processing for natural primary erotic rewards and yields importance for the neurochemical systems of addictive disorders including gambling disorder.

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