The cannabinoid receptor 1 (CB1) and transient receptor potential cation channel subfamily V member 1 (TRPV1) are proposed to mediate opposite behavioural responses. Their common denominator is the endocannabinoid ligand anandamide (AEA), which is believed to mediate antidepressant-like effect via CB1-R stimulation and depressive-like effect via TRPV1 activation. This is supposed to explain the bell-shaped dose-response curve for anandamide in preclinical models.

We investigated this assumption by administering the dual inhibitor of AEA hydrolysis and TRPV1 activation N-arachidonoyl-serotonin (AA-5HT) into the medial prefrontal cortex of rats. AA-5HT was given in three different doses (0.125, 0.250, 0.500 nmol/0.4 µl/side) and rat behaviour was assessed in the forced swim test.

Our results show significant antidepressant-like effect of AA-5HT (0.250 nmol) but no effects of low or high doses. The effect of 0.250 nmol AA-5HT was partially attenuated when coadministering the inverse CB1-agonist rimonabant (1.6 µg).

A 0.250 nmol of AA-5HT administration into the medial prefrontal cortex induced a significant antidepressant-like effect that was partially attenuated by locally blocking CB1-receptor.

To investigate whether specific symptoms of attention deficit hyperactivity disorder (ADHD) can help identify ADHD patients with mind wandering.

Subjects were adults ages 18–55 of both sexes (n=41) who completed the Mind-Wandering Questionnaire (MWQ) and the ADHD module of the Schedule for Affective Disorders and Schizophrenia for School-Age Children Epidemiologic Version. We used Spearman’s rank correlation and Pearson’s χ2 analyses to examine associations between the ADHD module and the MWQ and receiver operator characteristic (ROC) analyses to evaluate the diagnostic efficiency of the ADHD module.

Out of the three ADHD domains, the inattentive ADHD scores had the strongest association with the MWQ (total: r s=0.34, df=39, p=0.03; inattentive: r s=0.38, df=39, p=0.02; Hyperactive: r s=0.17, df=39, p=0.28). Correlation analyses between individual items on the ADHD module and the MWQ showed that two inattention items (‘failure to pay attention to detail’ and ‘trouble following instructions’) were positively associated with total scores on the MWQ (p=0.02). These two inattention items had the strongest association with the MWQ (r s=0.45, df=38, p=0.004). ROC analyses showed that the combined score of the two significant inattention items had the highest efficiency (AUC=0.71) in classifying high-level mind wanderers as defined by scores greater than the median split on the MWQ. The combined score of the two inattention items best identified high-level mind wanderers.

Results suggest a way to operationalise mind wandering using the symptoms of ADHD.

This study aimed to explore effects of adjunctive N-acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression.

We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment.

NAC treatment significantly improved depressive symptoms on the Montgomery–Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment.

Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.

The aim of this study was to investigate the degree of risk of maternal postpartum depression during the second month of puerperium.

In total, 387 postnatal women filled out a questionnaire concerning their health and social status, as well as the following tests: the Edinburgh Postnatal Depression Scale (EPDS), the Patient Health Questionnaire-9 (PHQ-9), the Neo Five-Factor Inventory (NEO-FFI) Personality Inventory and the Berlin Social Support Scales. After 4–8 weeks, patients responded to another questionnaire with the EPDS and the PHQ-9.

In total, 48 patients (12.40%) were found to be at risk of postpartum depression between the fourth and eighth weeks after delivery. Premenstrual syndrome [adjusted odds ratio (ORa)=2.93, confidence interval (CI) 1.30–6.63] and EPDS>12 points during the first week after the delivery (ORa=3.74, CI 1.59–9.04) increased the risk of postnatal depression. A similar role is played by a high result in neuroticism scale of the NEO-FFI (ORa=1.50, CI 1.17–1.92) and a positive family history of any psychiatric disorder (ORa=1.03, CI 1.01–1.06).

A history of premenstrual syndrome and a higher risk of affective disorder soon after a childbirth are associated with greater chances of depressive symptoms in the second month postpartum. This is also the case if a patient is neurotic and has a relative with a history of any psychiatric disorder. Such women should have their mental status carefully evaluated.

This study was conducted to investigate and clinically assess comorbid depression and its relevance in individuals suffering from gambling disorders. The DSM-V defines the condition of gambling disorder as a persistent and recurrent problematic gambling behaviour leading to clinically significant impairment or distress.

A total of 61 subjects with gambling disorders were assessed using the Structured Clinical Interview for the DSM-IV (SCID-I), the South Oaks Gambling Screen (SOGS) and the Major Depression inventory (MDI).

Two-way analysis of variance showed highly significant treatment outcomes associated with reductions in SOGS, F(1,60)=84.79, p<0.0001, MDI, F(1,60)=38.13, p<0.0001, craving, F(1,60)=29.59, p<0.0001, and gambling control, 47.65, p<0.0001. There was also a highly significant outcome associated with comorbidity in MDI, F(1,60)=9.17, p<0.0001. Finally, there was a significant interaction effect between treatment outcome and comorbidity, F(1,60)=3.90, p<0.005, suggesting that both treatment and comorbidity contributed to reductions in depressive symptoms.

These results suggest and highlights the importance and benefits of integrated treatment of gambling disorders and its comorbidity, but also stresses the importance of adequate screening and detection of these two variables.

Electroconvulsive therapy (ECT) is one of the most efficient treatments for major depression. Electroconvulsive seizures (ECS), the animal model of ECT, is widely used to study both mechanisms of action and adverse effects of ECT. As the treatment itself serves as an instant anaesthetic and anaesthetic agents may affect memory functions and behaviour, ECS is traditionally administered without muscle relaxation and anaesthesia. A major problem of unmodified ECS, which has only been addressed peripherally in the literature, is that some animals sustain spinal fractures and subsequent hind leg paralysis (paraplegia). This phenomenon leads to a higher degree of suffering and these animals need to be excluded from the studies. To reach sufficient statistical power, the group sizes are therefore often increased and this may lead to a pre-selected study group in risk of skewing the results. Moreover, the study design of the experiments do not comply with the 3R principles, which advocate for both refinement and reduction of animal experiments. The objective of this study is to systematically evaluate injuries caused by ECS.

We summarise the incidence of spinal fractures from 24 studies conducted during 2009–2015 in six different rat strains and report preliminary findings on scapular fractures following auricular ECS.

In total, 12.8% of all tested animals suffered from spinal fractures and we find an increase in spinal fracture incidence over time. Furthermore, X-ray analyses revealed that some animals displayed scapular fractures.

We discuss consequences of and possible explanations for ECS-induced fractures. Modifications of the method are highly warranted and we furthermore suggest that all animals are thoroughly examined for discrete fractures.

Recent studies have detected similarities between autism spectrum disorder and schizophrenia. We investigated structural abnormalities associated with autistic-like traits in patients with schizophrenia by voxel-based morphometry.

Patients with schizophrenia and healthy subjects were evaluated by the adult version of the social responsiveness scale (SRS-A), which is sensitive to autistic traits and symptoms even under subthreshold conditions, and magnetic resonance imaging.

There were significant decreases in the anterior cingulate cortex, bilateral hippocampi, cerebellums, and right insula of patients with schizophrenia, compared with healthy subjects. We found significant negative correlations of the social communication and interaction (SCI) score, a subscale of SRS-A, with grey matter volume in the left posterior superior temporal region of schizophrenia patients. When subscales of SCI were examined separately in schizophrenic patients, negative correlations were observed between the social cognition score and the volumes of the left posterior superior temporal region, and between social motivation and the posterior cingulate cortex.

We found significant negative correlation between the SCI score and the grey matter volume in the left posterior superior temporal region of schizophrenia patients. This area was the region affected in previous studies of autistic spectrum disorders. Further, this area was associated with the theory of mind. Schizophrenia patients not necessarily show the impairment of SCI, nor this correlated region was not always the point with schizophrenia-specific change. However, we reveal the relationship between the left posterior superior temporal gyrus and the severity of the SCI in schizophrenia by using with SRS-A.