The influence of personality traits on suicidal behaviour risk has been well documented. Personality traits and suicidal behaviour are partially genetically determined and personality has been described as an endophenotype of suicidal behaviour. The aim of this study was to investigate a possible association between personality traits with suicidal behaviour and selected serotonergic gene polymorphisms.

In the study we included 156 patients meeting DSM-IV criteria for bipolar disorder (BP) and 93 healthy controls. The personality dimensions were assessed using the Temperament and Character Inventory (TCI). We genotyped two selected polymorphisms of the tryptophan hydroxylase 1 (TPH1) gene (rs1800532 218A>C and rs1799913 779A>C) and polymorphism in the promoter region of serotonin transporter gene (5-HTTLPR, rs25531) related to serotoninergic neurotransmission. Multiple poisson regression, logistic regression and Kruskal–Wallis tests were applied.

We found numerous differences between the BP patients and the control group in terms of their TCI dimensions/subdimensions. Significant differences were found between patients with, and without, suicidal attempts in fatigability and asthenia (Ha4), as well as in harm avoidance (Ha). We also found that the interactions between TCI subdimensions (the interaction of disordiness (Ns4) and spiritual acceptance (St3), disordiness (Ns4) and integrated conscience (C5), extravagance (Ns3) and resourcefulness (Sd3)) were significantly contributing for suicidal behaviour risk. We found association between all studied genetic polymorphisms and several TCI dimensions and subdimensions.

Our results confirm that personality traits are partially determined by genes. Both personality traits and the interactions between temperament and character traits, may be helpful in predicting suicidal behaviour.

The neuropeptides oxytocin (OT) and arginine vasopressin (AVP) play important and interrelated roles in modulating mammalian social behaviour. While the OT system has received considerable research attention for its potential to treat psychiatric symptoms, comparatively little is known about the role of the AVP system in human social behaviour. To better understand the intraindividual stability of basal AVP, the present study assessed the reproducibility of basal plasma AVP concentrations.

Basal plasma AVP was assessed at four sampling points separated by 8 days, on average, in 16 healthy adult males.

Only one out of six comparisons revealed strong evidence for reproducibility of basal AVP concentrations (visit 2 vs. visit 4: r=0.8, p<0.001; all other comparisons p>0.1). The concordance correlation coefficient [0.15, 95% CI (−0.55, 0.73)] also revealed poor overall reproducibility.

Poor reliability of basal AVP concentrations suggests future work covarying AVP with trait markers should proceed with careful consideration of intraindividual fluctuations.

Dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis has been reported in depression. The aim was to investigate the potential association between depression and seven genes regulating or interfering with the HPA axis, including the gene encoding angiotensin converting enzyme (ACE).

In total, 78 single nucleotide polymorphisms (SNPs) and one insertion/deletion polymorphism were genotyped. The study included 408 individuals with depression and 289 controls. In a subset of cases, the interaction between genetic variants and stressful life events (SLEs) was investigated.

After quality control, 68 genetic variants were left for analyses. Four of nine variants within ACE were nominally associated with depression and a gene-wise association was likewise observed. However, none of the SNPs located within AVP, CRH, CRHR1, CRHR2, FKBP5 or NC3C1 were associated with depression. One nominally significant interaction, most likely due to chance, was identified.

The results indicate that ACE could be a potential candidate gene for depression.

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.