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Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterised by deficits in social behaviour, increased repetitive behaviour, anxiety and gastrointestinal symptoms. The aetiology of ASD is complex and involves an interplay of genetic and environmental factors. Emerging pre-clinical and clinical studies have documented a potential role for the gut microbiome in ASD, and consequently, the microbiota represents a potential target in the development of novel therapeutics for this neurodevelopmental disorder. In this study, we investigate the efficacy of the live biotherapeutic strain, Blautia stercoris MRx0006, in attenuating some of the behavioural deficits in the autism-relevant, genetic mouse model, BTBR T+ Itpr3tf/J (BTBR). We demonstrate that daily oral administration with MRx0006 attenuates social deficits while also decreasing repetitive and anxiety-like behaviour. MRx0006 administration increases the gene expression of oxytocin and its receptor in hypothalamic cells in vitro and increases the expression of hypothalamic arginine vasopressin and oxytocin mRNA in BTBR mice. Additionally at the microbiome level, we observed that MRx0006 administration decreases the abundance of Alistipes putredinis, and modulates the faecal microbial metabolite profile. This alteration in the metabolite profile possibly underlies the observed increase in expression of oxytocin, arginine vasopressin and its receptors, and the consequent improvements in behavioural outcomes. Taken together, these findings suggest that the live biotherapeutic MRx0006 may represent a viable and efficacious treatment option for the management of physiological and behavioural deficits associated with ASD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)

The realisation that microbes regarded as beneficial to the host can impart effects at sites distant from their habitat, has raised many possibilities for treatment of diseases. The objective of a workshop hosted in Turku, Finland, by the International Scientific Association for Probiotics and Prebiotics, was to assess the evidence for these effects and the extent to which early life microbiome programming influences how the gut microbiota communicates with distant sites. In addition, we examined how probiotics and prebiotics might affect the skin, airways, heart, brain and metabolism. The growing levels of scientific and clinical evidence showing how microbes influence the physiology of many body sites, leads us to call for more funding to advance a potentially exciting avenue for novel therapies for many chronic diseases.

Disruption of bacterial colonization during the early postnatal period is increasingly being linked to adverse health outcomes. Indeed, there is a growing appreciation that the gut microbiota plays a role in neurodevelopment. However, there is a paucity of information on the consequences of early-life manipulations of the gut microbiota on behavior. To this end we administered an antibiotic (vancomycin) from postnatal days 4-13 to male rat pups and assessed behavioral and physiological measures across all aspects of the brain-gut axis. In addition, we sought to confirm and expand the effects of early-life antibiotic treatment using a different antibiotic strategy (a cocktail of pimaricin, bacitracin, neomycin; orally) during the same time period in both female and male rat pups. Vancomycin significantly altered the microbiota, which was restored to control levels by 8 weeks of age. Notably, vancomycin-treated animals displayed visceral hypersensitivity in adulthood without any significant effect on anxiety responses as assessed in the elevated plus maze or open field tests. Moreover, cognitive performance in the Morris water maze was not affected by early-life dysbiosis. Immune and stress-related physiological responses were equally unaffected. The early-life antibiotic-induced visceral hypersensitivity was also observed in male rats given the antibiotic cocktail. Both treatments did not alter visceral pain perception in female rats. Changes in visceral pain perception in males were paralleled by distinct decreases in the transient receptor potential cation channel subfamily V member 1, the α-2A adrenergic receptor and cholecystokinin B receptor. In conclusion, a temporary disruption of the gut microbiota in early-life results in very specific and long-lasting changes in visceral sensitivity in male rats, a hallmark of stress-related functional disorders of the brain-gut axis such as irritable bowel disorder., (Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.)

Stress and genetic predisposition are two of the major risk factors for a variety of psychiatric illnesses. Inbred mouse strains are considered useful tools in dissecting the genetic basis of complex disorders. Indeed, mice of the C57BL/6 and BALB/c strains, differing markedly in anxiety behaviours, are among the most widely used in psychopharmacological research. However, there is a paucity of studies investigating the impact of social stress in these two strains. Moreover, whether these two mouse strains exhibit different sensitivities to chronic social defeat stress remains poorly studied. Thus in this study we compared the impact of repeated (10 days) social defeat stress on a variety of behavioural and endocrine parameters including social interaction, locomotor activity, plasma corticosterone, body weight and stress-related physiological parameters in both mouse strains. Given that the duration of stress exposure may differentially affect such responses we also compared stressors of short (Social Defeat-Short; SD-S) and of long (Social Defeat-Long; SD-L) duration. Our results show that although mice from both strains were defeated in both social defeat paradigms, only BALB/c mice displayed social interaction impairments following SD-S, whereas both strains were behaviourally sensitive to SD-L. Moreover, both strains also differed in some of the physiological alterations induced by social defeat stress. Specifically, SD-S did not induce any change in corticosterone levels in either of the two strains, whereas SD-L was able to induce significant changes in C57BL/6 mice only. SD-S induced differential effects on bodyweight gain in both strains, increasing it in C57BL/6 and decreasing it in BALB/c mice, whereas SD-L had no effect. On the other hand, exposure to SD-S resulted in cardiac hypertrophy in C57BL/6 mice and SD-L induced spleen hypertrophy and thymus atrophy in BALB/c mice in addition to decreasing faecal output. Overall, the innately anxious BALB/c mice were more sensitive to social stress than C57BL/6, with differential behavioural and physiological alterations emerging as a function of stress severity. These data suggest different coping strategies to social interaction stress between the two mouse strains. The genetic basis of this stress-resilience/susceptibility warrants further investigation., (Copyright © 2011 IBRO. Published by Elsevier Ltd. All rights reserved.)

This study investigated the key aspects of a successful integration experience into mental health nursing from the perspectives of new nurses working in a psychiatric institution. Analysis of 10 semistructured interviews revealed that the relational atmosphere in which new nurses find themselves is determinant of their satisfaction with their integration experience. Quality relational connections with patients constitute the primary motivation of new nurses in choosing a career in mental health. At the same time, quality relational connections between and among team members sustain such motivation. Conversely, a negative relational atmosphere sets the stage for new nurses to experience disillusionment and despair., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The neurokinin 3 (NK3) receptor is a novel target under investigation for improvement of symptoms of schizophrenia, because of its ability to modulate dopaminergic signaling. To further understanding of the function of this receptor, sensitivity to dopaminergic stimuli and levels of dopaminergic receptors and tyrosine hydroxylase in NK3 receptor knockout mice were studied. Knockout of the receptor was confirmed by lack of NK3 protein and lack of electrophysiological responsivity of presumed dopaminergic neurons to senktide. NK3 receptor knockout mice showed mild hyperlocomotion and deficits on the rotarod. NK3 receptor knockout mice did not show significant differences in sensitivity to locomotor effects of acute amphetamine (0.3, 1, and 3 mg/kg subcutaneously) or significant alterations in sensitization to locomotor effects of amphetamine, but did show nonsignificant hyperreactivity to 1 mg/kg amphetamine and a nonsignificantly increased propensity to develop sensitization. A small decrease in D1 receptor binding was seen in the dorsal striatum and olfactory tubercle, and a small decrease of in tyrosine hydroxylase in the olfactory tubercle, but no change was seen in D2 receptor binding. Together, these results support a role for the NK3 receptor in reactivity to dopaminergic stimuli, but the lack of robust changes indicates that the sensitivity to dopamine may be activity-dependent or benign in nature.