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  1. Home
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Browsing by Subject "Chronic stress"

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    Role of stress-related glucocorticoid changes in astrocyte-oligodendrocyte interactions that regulate myelin production and maintenance
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Miguel Hidalgo, José Javier
    Repeated activation of stress responses and elevated corticosteroids result in alterations of neuronal physiology and metabolism, and lead to disturbances of normal connectivity between neurons in various brain regions. In addition, stress responses are also associated with anomalies in the function of glial cells, particularly astrocytes and oligodendrocytes, which in turn may further contribute to the mechanisms of neuronal dysfunction. The actions of corticosteroids on astrocytes are very likely mediated by the presence of intracellular and cell membrane-bound CORT receptors. Although apparently less abundant than in astrocytes, activation of CORT receptors in oligodendrocytes also leads to structural changes that are reflected in myelin maintenance and plasticity. The close interactions between astrocytes and oligodendrocytes through extracellular matrix molecules, soluble factors and astrocyte-oligodendrocyte gap junctions very likely mediate part of the disturbances in myelin structure, leading to plastic myelin adaptations or pathological myelin disruptions that may significantly influence brain connectivity. Likewise, the intimate association of the tips of some astrocytes processes with a majority of nodes of Ranvier in the white matter suggest that stress and overexposure to corticosteroids may lead to remodeling of node of Ranvier and their specific extracellular milieu
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    The effect of chronic stress and obesity on sperm quality and testis histology in male rats; a morphometric and immunohistochemical study
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Demirci, Tuba; Sahin, Elvan
    Objective. Stress and obesity lead structural and functional abnormalities in many organs. This research investigated the effect of these two risk factors on sperm parameters and histologic structure of testis in rat model. Materials and methods. Twenty-four male rats were divided into four groups with six rats in each group as control, stress, obesity, and stress-obesity groups. The rats of obesity and stress-obesity groups were fed highfat diet for 12-week and obesity was created. Control and stress groups were given standard rat chow for the same time. Through last 4-week, stress and stressobesity groups were applied to chronic mild stress procedure. At the end of the experiment, epididymal sperm was collected from vas deferens and testes were harvested from sacrificed animals. Sperm samples were evaluated in terms of concentration and motility by using Makler Chamber. Sperm smears were stained with Eosin-Y stain for morphological evaluation, and also histochemically for GABA transporter-1 (GAT1) expression assessment. Testis sections were dyed with Hematoxylin-Eosin and Johnsen scores were assessed. GAT1 expression was detected in testis sections by immunohistochemistry, and TUNEL method was used for determining apoptosis in testis. Results. In comparison with the control samples in stress, obesity, and stress-obesity groups sperm concentration and motility decreased, and also the number of sperm with abnormal morphology increased. Stress, obesity, and stress-obesity groups showed a significantly decreased in sperm concentration and motility in comparison with the control group, and also in these groups had significantly increased number of abnormal sperm compared to control. Additionally, the testicular structure was deteriorated, and Johnsen scores decreased. And also GAT1 expression and apoptosis were prominent. These negative results, especially, testicular weight, sperm concentration, and Johnsen score were more observed in the stress-obesity group. Conclusions. Stress and obesity may induce male infertility by disrupting both sperm quality and testis histology. When stress and obesity are coexisting, these adverse effects are more severe. And also, increased GAT1 expression may be associated with these effects.

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