Humans have lived in a dynamic environment fraught with potential dangers for thousands of years. While fear and stress were crucial for the survival of our ancestors, today, they are mostly considered harmful factors, threatening both our physical and mental health. Trauma is a highly stressful, often life-threatening event or a series of events, such as sexual assault, war, natural disasters, burns, and car accidents. Trauma can cause pathological metaplasticity, leading to long-lasting behavioral changes and impairing an individual’s ability to cope with future challenges. If an individual is vulnerable, a tremendously traumatic event may result in post-traumatic stress disorder (PTSD). The hypothalamus is critical in initiating hormonal responses to stressful stimuli via the hypothalamic–pituitary–adrenal (HPA) axis. Linked to the prefrontal cortex and limbic structures, especially the amygdala and hippocampus, the hypothalamus acts as a central hub, integrating physiological aspects of the stress response. Consequently, the hypothalamic functions have been attributed to the pathophysiology of PTSD. However, apart from the well-known role of the HPA axis, the hypothalamus may also play different roles in the development of PTSD through other pathways, including the hypothalamic–pituitary–thyroid (HPT) and hypothalamic–pituitary–gonadal (HPG) axes, as well as by secreting growth hormone, prolactin, dopamine, and oxytocin. This review aims to summarize the current evidence regarding the neuroendocrine functions of the hypothalamus, which are correlated with the development of PTSD. A better understanding of the role of the hypothalamus in PTSD could help develop better treatments for this debilitating condition.

Objectives: Lipid peroxidation and hyperglycemia are common signs for diabetes. Natural antioxidants such as Spirulina platensis microalgae (SPM) may prevent lipid peroxidation and hyperglycemia. This study aimed to evaluate the effects of SPM on antioxidant and anti-inflammatory in diabetic rats. Materials and methods: Sixty-four rats were divided into eight groups (n=8) and orally treated with 0, 10, 20 and 30 mg/kg body weight of SPM extract. Experimental groups included diabetic rats fed with 0 (DC), 10, 20 and 30 mg/kg SPM. Healthy rats were treated with 0 mg/kg SPM (HC), 10 mg/kg SPM, 20 mg/kg SPM and 30 mg/kg SPM. At the end of the trial, blood samples were collected and the plasma concentrations of trace minerals (TMs), biochemical parameters, and antioxidant enzymes in liver were evaluated. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), TNF-α (tumor necrosis factor-alpha) and IL-6 (interleukin-6) were evaluated. Results: Our findings showed that diabetes significantly lowered the plasma concentration of TMs and antioxidant enzymes in liver and also increased the levels of malondialdehyde, glucose, lipid profile, AST, ALT, TNF-α and IL-6 (DC vs HC). However, an oral supplement of SPM (20 and 30 mg/kg body weight) lowered levels of malondialdehyde level, glucose, lipid parameters, AST, ALT, TNF-α and IL-6. The same levels increased the plasma contents of zinc, iron, copper and selenium and activity of antioxidant enzymes (P<0.05). Conclusion: It can be concluded that diabetes decreases TM concentration and antioxidant enzymes and also increases lipid profile, glucose, AST, ALT, TNF-α and IL-6 concentrations. Inclusion of SPM supplementing (20 and 30 mg/kg body weight) increased some TMs and antioxidant enzymes. SPM may provide TMs for synthesis of antioxidant enzymes which subsequently reduce lipid profile, glucose concentration and anti-inflammatory responses.

Emerging evidence supports the gut microbiota and the brain communication in general health. This axis may affect behavior through modulating neurotransmission, and thereby involve in the pathogenesis and/or progression of different neuropsychiatric disorders such as depression. Brain-derived neurotrophic factor and cAMP response element-binding protein known as CREB/BDNF pathway plays have critical functions in the pathogenesis of depression as the same of mechanisms related to antidepressants. However, the putative causal significance of the CREB/BDNF signaling cascade in the gut-brain axis in depression remains unknown. Also interventions such as probiotics supplementation and exercise can influence microbiome also improve bidirectional communication of gut and brain. In this review we aim to explain the BDNF/CREB signaling pathway and gut microbiota dysfunction and then evaluate the potential role of probiotics, prebiotics, and exercise as a therapeutic target in the gut microbiota dysfunction induced depression. The current narrative review will specifically focus on the impact of exercise and diet on the intestinal microbiota component, as well as the effect that these therapies may have on the microbiota to alleviate depressive symptoms. Finally, we look at how BDNF/CREB signaling pathway may exert distinct effects on depression and gut microbiota dysfunction.

Background and Purpose: Ample evidence indicates that chronic adolescence stress is associated with an increased risk of developing neuropsychiatric disorders in adulthood. Given the importance of the effective therapeutic ways to overcome adolescent stress-related deficits, the present study investigated the effects of Spirulina platensis (SP), environmental enrichment (EE), and voluntary exercise (EX) and their combination on anxiety or depression-like behaviors, oxidative stress, and alterations of BDNF and 5HT-3 receptors in the prefrontal cortex (PFC) induced by adolescent stress in adult female rats. Methods: During the adolescent period (PNDs30-40), rats were subjected to restraint stress. Then, the animals were subjected to SP treatment (200 mg/kg/day), EX, EE, and the combined treatments (SP+EX, and SP+EE) for 15 days between PNDs41-55. Subsequently, anxiety or depression-like behaviors, BDNF levels, oxidative stress markers and mRNA expression of BDNF and 5HT₃ in the PFC were assessed. Results: Stressed rats demonstrated enhanced anxiety levels and depression-like behaviors in adulthood. Regarding the oxidative stress markers, stressed rats exhibited significantly higher levels of malondialdehyde, a lipid peroxidation product, higher activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) and significantly lower total antioxidant reactivity capacity in the PFC. Additionally, adolescent stress significantly increased 5HT3 receptor mRNA expression and decreased BDNF content and its mRNA expression in the PFC. Treatments with SP, EX, EE, and the combined interventions alleviated these deficits. Conclusion: Our findings indicate that appropriate interventions during the adolescent period can protect against adolescent stress-induced behavioral, and biochemical defects and oxidative stress damage in adulthood.