Non-human contributions to personality neuroscience: From fish through primates - a concluding editorial overview.

This special issue attempts to integrate personality, psychopathology, and neuroscience as means to improve understanding of specific traits and trait structures in humans. The key strategy is to dive into comparative research using a range of species to provide simple models. This strategy has, as its foundation, the fact that the most basic functions, and their supporting neural systems, are highly conserved in evolution. The papers collected in the issue show that, from fish, through rats, to primates, the homologies in brain systems and underlying functions (despite species-specific forms of expression) allow simpler cases to provide insights into the neurobiology behind more complex ones including human. Our introductory editorial paper to this special issue took a bottom-up approach, starting with the genetics of conserved brain systems and working up to cognition. Here, we deconstruct the different aspects of personality, progressing from more complex ones in primates to least complex in fish. With the primate section, we summarize papers that discuss the factors that contribute to sociability in primates and how they apply to healthy and pathological human personality traits. In the rat section, the focus is driven by psychopathology and the way that "high" strains selected for extreme behaviors can illuminate the neurobiology of motivated responses to environmental cues. The section on fish summarizes papers that look into the most fundamental emotional reactions to the environment that are governed by primitive and conserved brain structures. This raises metatheoretical questions on the nature of traits and to a section that asks "which animals have personalities." We believe that the issue as a whole provides a nuanced answer to this question and shines a new, comparative, light on the interpretation of personality structure and the effects on it of evolution.

The association between the renin-angiotensin system and the hypothalamic-pituitary-adrenal axis in anxiety disorders: A systematic review of animal studies.

Anxiety is characterized as the emotional response in anticipation of a future threat. This hypervigilant state comprehends a cascade of neuroendocrine and physiological processes, involving the renin-angiotensin system (RAS) and hypothalamic-pituitary-adrenal axis (HPA). Excessive and chronic anxiety may ultimately lead to the development of anxiety disorders. This systematic review aimed to investigate experimental studies using animal models that explored the relationship between RAS and the HPA axis in anxiety disorders. A systematic search was conducted in MEDLINE/PubMed, Embase and Web of Science, and was performed according to PRISMA guidelines. The inclusion criteria was mainly the mention of RAS, HPA axis, and an anxiety disorder in the same study. Quality of studies was evaluated according to the table of risk of bias from SYRCLE. From 12 eligible studies, 7 were included. Research in rats and mice shows that the overactivation of the RAS and HPA axis triggers several neuroendocrine reactions, mainly mediated by AT1 receptors, which promote anxiety-like behaviors and positive feedback for its hyperactivation. On the contrary, the administration of antihypertensive drugs, such as angiotensin AT1 receptor blocker, propitiated the regulation of the RAS and HPA axis, maintaining homeostasis even amid aversive situations. Assessment of risk of bias revealed a pronounced unclear to high risk in several categories, which thus jeopardize the comparability and reproducibility of the results. Nonetheless, the preclinical evidence indicates that the hyperactivation of both RAS and HPA axis during stress exerts deleterious consequences, inducing anxiogenic responses. Moreover, the compiled results show that the modulation of both systems by the administration of AT1 receptor blockers produce anxiolytic effects in animal models and may constitute a new venue for the treatment of anxiety-like disorders.

Effect of chronic unpredictable mild stress on the expression profile of serotonin receptors in rats and mice: a meta-analysis.

Chronic-stress-induced depression is recognized as a widespread public health concern. Selective serotonin reuptake inhibitors (SSRIs) have been the most common treatment for this illness. However, the role of 5-hydroxytryptamine (5-HT) receptor subtypes in stress-induced depression remains unclear. Evidence from Animal studies has reported a variety of results regarding the effects of chronic unpredictable mild stress (CUMS) on serotonin signaling pathways and 5-HT receptor subtypes. This divergence may rely on differences in protocols, methods, and studied pathways. Thus, the aim of this systematic review was to weigh the currently available findings regarding serotonin receptor changes in animal models of CUMS. Overall, our meta-analysis results showed the association of altered expression of 5-HT1A receptors in the frontal cortex and 5-HT2A receptors both in the whole cortex and the hypothalamus of rats following CUMS. Moreover, by using a qualitative-structured analysis and the application of risk-of-bias tools, we identified possible sources of data variation between the studied literature, which should be taken into account in future animal studies of chronic-stress induced depression.