Neuroscience
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Astrocytes experience significant metabolic shifts in the "sensitive period" of neurological function recovery following cerebral ischemia. However, the changes in astrocyte lipid metabolism and their implications for neurological recovery remain unknown. In the present study, we employed a mouse middle cerebral artery occlusion model to investigate the changes in de novo lipogenesis and interleukin-33 (IL-33) production in astrocytes and elucidate their role in blood-brain barrier (BBB) repair in the subacute phase of cerebral ischemia. ⋯ Inhibition of lipogenesis in astrocytes decreased IL-33 production in the peri-infarct area, deteriorated BBB damage and interfered with neurological recovery. In addition, supplementation of IL-33 alleviated BBB destruction and improved neurological recovery worsened by lipogenesis inhibition. These findings indicate that astrocyte lipogenesis increases the production of IL-33 in the peri-infarct area, which promotes BBB repair in the subacute phase of cerebral ischemia injury and improves long-term functional recovery.
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We explored the phenomenon of unintentional force drifts in the absence of visual feedback. Based on the idea of direct force control with internal models and on the idea of indirect force control with referent coordinates to the involved muscle groups, contrasting predictions were drawn for changes in the drift magnitude when acting against external spring loads. Fifteen young subjects performed typical accurate force production tasks by pressing with the Index finger at 20% of maximal voluntary contraction (MVC) in isometric conditions and while acting against one of the three external springs with different stiffness. ⋯ We view these observations as strong arguments in favor of the theory of control with spatial referent coordinates. In particular, force drifts were likely consequences of drifts of referent coordinates to both agonist and antagonist muscles. The lack of drift effects on both perception-to-report and perception-to-act fit the scheme of kinesthetic perception based on the interaction of efferent (referent coordinate) and afferent processes.
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Fragmentation of the daily sleep-wake rhythm with increased nighttime awakenings and more daytime naps is correlated with the risk of development of Alzheimer's disease (AD). To explore whether a causal relationship underlies this correlation, the present study tested the hypothesis that chronic fragmentation of the daily sleep-wake rhythm stimulates brain amyloid-beta (Aβ) levels and neuroinflammation in the 3xTg-AD mouse model of AD. Female 3xTg-AD mice were allowed to sleep undisturbed or were subjected to chronic sleep fragmentation consisting of four daily sessions of enforced wakefulness (one hour each) evenly distributed during the light phase, five days a week for four weeks. ⋯ Sleep fragmentation also stimulated neuroinflammation as shown by increased expression of markers of microglial activation and proinflammatory cytokines measured by q-RT-PCR analysis of hippocampal samples. No significant effects of sleep fragmentation on Aβ, tau, or neuroinflammation were observed in the cerebral cortex. These studies support the concept that improving sleep consolidation in individuals at risk for AD may be beneficial for slowing the onset or progression of this devastating neurodegenerative disease.