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      Effect of Intermittent Feeding on Gonadal Function in Male And Female NMRI Mice During Chronic Stress

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          Abstract

          ABSTRACT Stress can inhibit gonadal activity via Hypothalamus-Pituitary-Gonad (HPG) axis activity suppression. In the present study, effects of intermittent feeding (IF) on gonadal function under stress in male and female mice were evaluated. Twenty eight male and twenty eight female mice's were divided into four groups. The control group received adequate food and water without stress. The second group received four days of electric shock without food deprivation. The third group was deprived of food two hours/day for a week, and the fourth group was deprived of food (2 hours/day for seven consecutive days) and then electric foot shock stress was applied to them for four days. Blood samples were collected from all animals for plasma testosterone, estrogen and/or Interlukin-6 (IL-6) evaluation. The animals’ gonads were also removed and fixed for the measure of their weight. Results showed that stress reduces both testosterone and estrogen levels, whereas IF did not change the hormone levels. In addition, stress increases blood IL-6 concentration. The combination of IF and stress, increased the hormone levels in animals. Stress and IF alone had no significant effect on gonadal weight in the male mice, whereas stress decreased gonadal weight in the females. Combination of stress with IF increased gonadal weight in both male and female mice. In conclusion stress showed a negative effect on gonadal function in both animals with more effect on females. Intermittent feeding inhibits the stress effect and even promotes the gonadal function in both sexes. The effect may be due to IL-6 reduction.

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          Stress and the brain: from adaptation to disease.

          In response to stress, the brain activates several neuropeptide-secreting systems. This eventually leads to the release of adrenal corticosteroid hormones, which subsequently feed back on the brain and bind to two types of nuclear receptor that act as transcriptional regulators. By targeting many genes, corticosteroids function in a binary fashion, and serve as a master switch in the control of neuronal and network responses that underlie behavioural adaptation. In genetically predisposed individuals, an imbalance in this binary control mechanism can introduce a bias towards stress-related brain disease after adverse experiences. New candidate susceptibility genes that serve as markers for the prediction of vulnerable phenotypes are now being identified.
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            The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission.

            Mounting evidence suggests that acute and chronic stress, especially the stress-induced release of glucocorticoids, induces changes in glutamate neurotransmission in the prefrontal cortex and the hippocampus, thereby influencing some aspects of cognitive processing. In addition, dysfunction of glutamatergic neurotransmission is increasingly considered to be a core feature of stress-related mental illnesses. Recent studies have shed light on the mechanisms by which stress and glucocorticoids affect glutamate transmission, including effects on glutamate release, glutamate receptors and glutamate clearance and metabolism. This new understanding provides insights into normal brain functioning, as well as the pathophysiology and potential new treatments of stress-related neuropsychiatric disorders.
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              Gonadal steroid hormone receptors and sex differences in the hypothalamo-pituitary-adrenal axis.

              The rapid activation of stress-responsive neuroendocrine systems is a basic reaction of animals to perturbations in their environment. One well-established response is that of the hypothalamo-pituitary-adrenal (HPA) axis. In rats, corticosterone is the major adrenal steroid secreted and is released in direct response to adrenocorticotropin (ACTH) secreted from the anterior pituitary gland. ACTH in turn is regulated by the hypothalamic factor, corticotropin-releasing hormone. A sex difference exists in the response of the HPA axis to stress, with females reacting more robustly than males. It has been demonstrated that in both sexes, products of the HPA axis inhibit reproductive function. Conversely, the sex differences in HPA function are in part due to differences in the circulating gonadal steroid hormone milieu. It appears that testosterone can act to inhibit HPA function, whereas estrogen can enhance HPA function. One mechanism by which androgens and estrogens modulate stress responses is through the binding to their cognate receptors in the central nervous system. The distribution and regulation of androgen and estrogen receptors within the CNS suggest possible sites and mechanisms by which gonadal steroid hormones can influence stress responses. In the case of androgens, data suggest that the control of the hypothalamic paraventricular nucleus is mediated trans-synaptically. For estrogen, modulation of the HPA axis may be due to changes in glucocorticoid receptor-mediated negative feedback mechanisms. The results of a variety of studies suggest that gonadal steroid hormones, particularly testosterone, modulate HPA activity in an attempt to prevent the deleterious effects of HPA activation on reproductive function.
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                Author and article information

                Journal
                babt
                Brazilian Archives of Biology and Technology
                Braz. arch. biol. technol.
                Instituto de Tecnologia do Paraná - Tecpar (Curitiba, PR, Brazil )
                1516-8913
                1678-4324
                2017
                : 60
                : e17160607
                Affiliations
                [2] Tehran orgnameBaqiyatallah University of Medical Sciences orgdiv1Neuroscience Research Center Iran
                [1] Tehran orgnameIslamic Azad University orgdiv1Department of Biology Iran
                Article
                S1516-89132017000100439 S1516-8913(17)06000000439
                10.1590/1678-4324-2017160607
                c48db387-d87c-4c16-8742-598a7d9aaf77

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 03 February 2016
                : 14 July 2016
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 39, Pages: 0
                Product

                SciELO Brazil

                Self URI: Full text available only in PDF format (EN)
                Categories
                Biological and Applied Sciences

                Testosterone,Estrogen,Gonad,IL-6,Intermittent Feeding,Stress
                Testosterone, Estrogen, Gonad, IL-6, Intermittent Feeding, Stress

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