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Institute
Aggression and deficient cognitive control problems are widespread in psychiatric disorders, including major depressive disorder (MDD). These abnormalities are known to contribute significantly to the accompanying functional impairment and the global burden of disease. Progress in the development of targeted treatments of excessive aggression and accompanying symptoms has been limited, and there exists a major unmet need to develop more efficacious treatments for depressed patients. Due to the complex nature and the clinical heterogeneity of MDD and the lack of precise knowledge regarding its pathophysiology, effective management is challenging. Nonetheless, the aetiology and pathophysiology of MDD has been the subject of extensive research and there is a vast body of the latest literature that points to new mechanisms for this disorder. Here, we overview the key mechanisms, which include neuroinflammation, oxidative stress, insulin receptor signalling and abnormal myelination. We discuss the hypotheses that have been proposed to unify these processes, as many of these pathways are integrated for the neurobiology of MDD. We also describe the current translational approaches in modelling depression, including the recent advances in stress models of MDD, and emerging novel therapies, including novel approaches to management of excessive aggression, such as anti-diabetic drugs, antioxidant treatment and herbal compositions.
What reaction stops revenge taking? Four experiments (total N = 191) examined this question where the victim of an interpersonal transgression could observe the offender's reaction (anger, sadness, pain, or calm) to a retributive noise punishment. We compared the punishment intensity selected by the participant before and after seeing the offender's reaction. Seeing the opponent in pain reduced subsequent punishment most strongly, while displays of sadness and verbal indications of suffering had no appeasing effect. Expression of anger about a retributive punishment did not increase revenge seeking relative to a calm reaction, even when the anger response was disambiguated as being angry with the punisher. It is concluded that the expression of pain is the most effective emotional display for the reduction of retaliatory aggression. The findings are discussed in light of recent research on reactive aggression and retributive justice.
During deployment, soldiers face situations in which they are not only exposed to violence but also have to perpetrate it themselves. This study investigates the role of soldiers' levels of posttraumatic stress disorder (PTSD) symptoms and appetitive aggression, that is, a lust for violence, for their engaging in violence during deployment. Furthermore, factors during deployment influencing the level of PTSD symptoms and appetitive aggression after deployment were examined for a better comprehension of the maintenance of violence. Semi‐structured interviews were conducted with 468 Burundian soldiers before and after a 1‐year deployment to Somalia. To predict violent acts during deployment (perideployment) as well as appetitive aggression and PTSD symptom severity after deployment (postdeployment), structural equation modeling was utilized. Results showed that the number of violent acts perideployment was predicted by the level of appetitive aggression and by the severity of PTSD hyperarousal symptoms predeployment. In addition to its association with the predeployment level, appetitive aggression postdeployment was predicted by violent acts and trauma exposure perideployment as well as positively associated with unit support. PTSD symptom severity postdeployment was predicted by the severity of PTSD avoidance symptoms predeployment and trauma exposure perideployment, and negatively associated with unit support. This prospective study reveals the importance of appetitive aggression and PTSD hyperarousal symptoms for the engagement in violent acts during deployment, while simultaneously demonstrating how these phenomena may develop in mutually reinforcing cycles in a war setting.
The negative societal impacts associated with the increasing prevalence of violence and aggression is increasing, and, with this rise, is the need to understand the molecular and cellular changes that underpin ultrasound-induced aggressive behavior. In mice, stress-induced aggression is known to alter AMPA receptor subunit expression, plasticity markers, and oxidative stress within the brain. Here, we induced aggression in BALB/c mice using chronic ultrasound exposure and examined the impact of the psychoactive anti-oxidant compounds thiamine (vitamin B1), and its derivative benfotiamine, on AMPA receptor subunit expression, established plasticity markers, and oxidative stress. The administration of thiamine or benfotiamine (200 mg/kg/day) in drinking water decreased aggressive behavior following 3-weeks of ultrasound exposure and benfotiamine, reduced floating behavior in the swim test. The vehicle-treated ultrasound-exposed mice exhibited increases in protein carbonyl and total glutathione, altered AMPA receptor subunits expression, and decreased expression of plasticity markers. These ultrasound-induced effects were ameliorated by thiamine and benfotiamine treatment; in particular both antioxidants were able to reverse ultrasound-induced changes in GluA1 and GluA2 subunit expression, and, within the prefrontal cortex, significantly reversed the changes in protein carbonyl and polysialylated form of neural cell adhesion molecule (PSA-NCAM) expression levels. Benfotiamine was usually more efficacious than thiamine. Thus, the thiamine compounds were able to counteract ultrasound-induced aggression, which was accompanied by the normalization of markers that have been showed to be associated with ultrasound-induced aggression. These commonly used, orally-active compounds may have considerable potential for use in the control of aggression within the community.
This article is part of the Special Issue entitled ‘Current status of the neurobiology of aggression and impulsivity’.
Rationale
While brain serotonin (5-HT) function is implicated in gene-by-environment interaction (GxE) impacting the vulnerability-resilience continuum in neuropsychiatric disorders, it remains elusive how the interplay of altered 5-HT synthesis and environmental stressors is linked to failure in emotion regulation.
Objective
Here, we investigated the effect of constitutively impaired 5-HT synthesis on behavioral and neuroendocrine responses to unpredictable chronic mild stress (CMS) using a mouse model of brain 5-HT deficiency resulting from targeted inactivation of the tryptophan hydroxylase-2 (Tph2) gene.
Results
Locomotor activity and anxiety- and depression-like behavior as well as conditioned fear responses were differentially affected by Tph2 genotype, sex, and CMS. Tph2 null mutants (Tph2\(^{−/−}\)) displayed increased general metabolism, marginally reduced anxiety- and depression-like behavior but strikingly increased conditioned fear responses. Behavioral modifications were associated with sex-specific hypothalamic-pituitary-adrenocortical (HPA) system alterations as indicated by plasma corticosterone and fecal corticosterone metabolite concentrations. Tph2\(^{−/−}\) males displayed increased impulsivity and high aggressiveness. Tph2\(^{−/−}\) females displayed greater emotional reactivity to aversive conditions as reflected by changes in behaviors at baseline including increased freezing and decreased locomotion in novel environments. However, both Tph2\(^{−/−}\) male and female mice were resilient to CMS-induced hyperlocomotion, while CMS intensified conditioned fear responses in a GxE-dependent manner.
Conclusions
Our results indicate that 5-HT mediates behavioral responses to environmental adversity by facilitating the encoding of stress effects leading to increased vulnerability for negative emotionality.