Corrigendum to: Effects of exercise on adolescent and adult hypothalamic and hippocampal neuroinflammation (Hippocampus, (2016), 26, (1435–1446), 10.1002/hipo22620)

© 2018 Wiley Periodicals, Inc. Published in Hippocampus 26:1435–1446 (2016) DOI: 10.1002/hipo22620 The authors of this article have notified us that one of the funding agencies was incorrectly acknowledged. The correct citation of the funding body is listed below: This work was supported by a Discovery Project Grant (DP130100508) and a Future Fellowship (FT110100084) from the Australian Research Council as well as an RMIT University Vice Chancellor's Senior Research Fellowship. We apologize for any inconvenience this may have caused

Effects of exercise on adolescent and adult hypothalamic and hippocampal neuroinflammation.

Adolescence is a period of significant brain plasticity that can be affected by environmental factors, including the degree of physical activity. Here we hypothesized that adolescent rats would be more sensitive to the beneficial metabolic and anti-inflammatory effects of voluntary exercise than adult rats, whose more mature brains have less capacity for plasticity. We tested this by giving adolescent and adult Wistar rats four weeks' voluntary access to running wheels. At the end of this period we assessed metabolic effects, including weight and circulating leptin and ghrelin, as well as performance in a novel object recognition test of memory and central changes in neuronal proliferation, survival, synaptic density, and inflammatory markers in hippocampus. We found exercise reduced fat mass and circulating leptin levels in both adults and adolescents but suppressed total weight gain and lean mass in adults only. Exercise stimulated neuronal proliferation in the suprapyramidal blade of the dentate gyrus in both adults and adolescents without altering the number of mature neurons during this time frame. Exercise also increased dentate microglial numbers in adolescents alone and microglial numbers in this region were inversely correlated with performance in the novel object recognition test. Together these data suggest that adolescent hippocampal microglia are more sensitive to the effects of exercise than those of adults, but this leads to no apparent improvement in recognition memory. This article is protected by copyright. All rights reserved

Eating behavior and stress: a pathway to obesity (Review)

Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body's resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie "palatable" food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society

The Role of Early Life Programming in Vulnerability and Resilience in Relation to HIV

Despite significant advances in HIV/AIDS research, the disease still impacts millions of people worldwide. The psychosocial environment of the patient plays an important role in the disease progression. Psychological stress, mental health issues and lack of social support contribute to a poor prognosis, particularly in those patients with prior exposure to these risk factors. Early life stress is known to affect mental health and modulate neuroendocrine and immune function long term, influencing individual's vulnerability to adult stress and compromised health status. This increased susceptibility to the adverse effects of stress may in turn promote the rate of HIV disease progression. Understanding the possible interactions between early life experiences of an infected individual and their ability to cope with the diagnosis and health consequences of HIV infection may shed light on the underlying biological mechanisms contributing to the disease progression and, thus, to improve current therapeutic strategies

Neuroinflammation and behaviour

No abstract availabl

Reducing resistance to diabetes treatment using short narrative interventions

Objective. This article presents a narrative-based technique, which allows medical personnel to empower patients with diabetes and improve adherence. Methods. The study was undertaken in Maccabi Healthcare Services, among 123 patients diagnosed with diabetes. Four empathic narratives were constructed, referring to different factors influencing resistance to treatment, as were identified by the Resistance to Treatment Questionnaire. Each narrative contains statements typical for patients whose resistance to treatment is influenced by a particular factor. An Empathic Narratives Evaluation Questionnaire was designed for this study. It contained three items, assessing the correlation of a specific empathic narrative with the patient's attitude and their reasons for resistance to treatment. The patients were asked to indicate whether they recognize these narratives as describing their reasons for resistance. Three empathic narratives were read to each patient: two narratives were matched for the two major categories of resistance for each patient and one narrative related to a category of resistance that received the lowest score. Results. The narratives were found to correspond to the core reasons for resistance to diabetes treatment. Significant difference was found also between the scores of the empathic narrative related to the second strongest reason for resistance to treatment and the empathic narrative related to the weakest reason for resistance to treatment. This finding supports testimonial validity of the narratives. Conclusion. Short narrative interventions demonstrated in this study can be used by health care professionals as a working tool that provides the possibility reducing the patient's reasons for resistance to treatment

Factors in early life programming of reproductive fitness

Fertility rates have been declining worldwide, with a growing number of young women suffering from infertility. Infectious and inflammatory diseases are important causes of infertility, and recent evidence points to the critical role of the early life microbial environment in developmental programming of adult reproductive fitness. Our laboratory and others have demonstrated that acute exposure to an immunological challenge early in life has a profound and prolonged impact on male and female reproductive development. This review presents evidence that perinatal exposure to immunological challenge by a bacterial endotoxin, lipopolysaccharide (LPS), acts at all levels of the hypothalamic-pituitary-gonadal (HPG) axis, resulting in long lasting changes in reproductive function, suggesting that disposition to infertility may begin early in lif

Transgenerational transmission of anxiety induced by neonatal exposure to lipopolysaccharide: Implications for male and female germ line

Neonatal lipopolysaccharide (LPS) exposure increases anxiety-like behaviour and alters neuroendocrine responses to stress in adult rats. The current study assessed whether this anxiety-related phenotype observed in rats neonatally exposed to LPS is transferable to subsequent generations. Wistar rats were exposed to LPS (0.05 mg/kg, Salmonella enteritidis) or non-pyrogenic saline (equivolume) on postnatal days 3 and 5. In adulthood, animals were subjected to restraint and isolation stress or no stress, and subsequently evaluated for anxiety-like behaviours on the elevated plus maze, acoustic startle response, and holeboard apparatus. Blood was collected to examine corticosterone responses to stress and behavioural testing in adulthood. Animals from both treatment groups which exhibited the anxiety-like phenotype were bred with untreated partners. Maternal care of the second generation (F2) was monitored over the first week of life. In adulthood, the F2 generation underwent identical testing procedures as the parental (F1) generation. The F2 offspring of females exposed to LPS as neonates exhibited an anxiety-like phenotype in adulthood and a potentiated corticosterone response to stress (p < .05). F2 offspring of males exposed to LPS as neonates also exhibited an anxiety-like phenotype (p < .05), however, no differences in corticosterone responses were observed. To determine the impact of maternal care on the anxiety-like phenotype, a cross-fostering study was conducted in which offspring of LPS-treated females were fostered to saline-treated mothers and vice versa, which was found to reverse the behavioural and endocrine phenotypes of the F2 generation. These data indicate that a neonatally bacterially induced anxiety phenotype is transferable across generations in both sexes. Maternal care is the mediating mechanism along the maternal line. We suggest that transmission may be dependent upon heritable epigenetic phenomena for the paternal line. The implications of this study apply to potential neuroimmune pathways through which psychopathology may be transmitted along filial lines