Neuroscience
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Physical exercise practice has been increasingly recommended in the prevention and treatment of chronic diseases, causing a positive effect from body weight/fat loss to improved cognitive function. Maternal exercise seems to induce the same positive lifelong adaptations to the offspring. We hypothesized that maternal exercise can prevent redox imbalance in adult offspring's hippocampus exposed to a high-fat diet (HFD). ⋯ In the hippocampus, both maternal exercise intensities could increase antioxidant defense. Hippocampal redox homeostasis was impaired by HFD, causing increased superoxide levels, which was prevented by exercise without load, while overload caused only a reduction of the effect. In summary, the practice of swimming exercise without overload during pregnancy seems to be more beneficial when evaluated in animal model, preventing HFD induced redox imbalance and increasing antioxidant defense while overload swimming exercise during pregnancy demonstrated a negative effect on offspring submitted to HFD consumption.
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Recent studies have demonstrated that programmed necrosis (necroptosis) is a delayed component of ischemic neuronal injury and our previous study has shown that pannexin 1 channel is involved in cerebral ischemic injury and cellular inflammatory response. Here, we examined whether the pannexin 1 channel inhibitor, 10panx, could reduce focal ischemic brain injury in rats by inhibiting cellular necroptosis and the associated inflammation. Male Sprague-Dawley rats were randomly divided into sham-operated, MCAO (transient middle cerebral artery occlusion) group, and 10panx-treated groups. ⋯ Immunent co-labeling of RIP3 with HMGB1 showed that RIP3 protein was closely related with the release of HMGB1 from nucleus to cytoplasm. Our data suggested that 10panx treatment may ameliorate MCAO injury by reducing RIP3-mediated necroptosis, HMGB1 release and associated inflammatory response. RIP3 may play an important role in the release of HMGB1 and inflammation after stroke.
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The platelet-derived growth factor receptor-α (PDGFRα) principally mediates growth factor signals in oligodendroglial progenitors and is involved in oligodendrogenesis and myelinogenesis in the developing spinal cord. However, the role of PDGFRα in the developing forebrain remains relatively unknown. We established a conditional knockout mouse for the Pdgfra gene (N-PRα-KO) using a Nestin promoter/enhancer-driven Cre recombinase and examined forebrain development. ⋯ After the defective PDGFRα signal in the forebrain, these phenotypes were clearly different from those in the spinal cord that showed defective populations expansion and migration of oligodendroglial lineage and premature myelination, as previously described. In contrast, areas of severe hypomyelination were common to both anatomical sites. PDGFRα was critically involved in the myelination of the forebrain and may differently regulate oligodendroglial lineage between the forebrain and spinal cord.