Neuroscience
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The aim of this study was to explore, during adolescence, alterations in the use of a sensori-motor representation as unveiled by the measurement of anticipatory postural control in a bimanual load-lifting task. We hypothesised that adolescence constitutes a period of refinement of anticipatory postural control due to on-going updates of the body schema and sensori-motor representations. The anticipatory postural control was assessed using a bimanual load-lifting paradigm in which subjects stabilise their left postural forearm, which is supporting an object, while they use their right hand to lift up the object. ⋯ The decrease of activity over postural flexors, which ensure postural stabilisation, appeared later in adolescents with respect to adults. Delayed timing adjustments and increased variability could reflect intense developmental processes underlain by an intense period of CNS maturation during adolescence. We discuss the role of brain maturation in the refinement of sensori-motor representations and the update of body schema.
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The aim of this study was to investigate whether an objective measure of freezing of gait (FOG) using a validated alternating stepping in place (SIP) task, is related to executive and/or visuospatial cognitive impairment in Parkinson's disease (PD). ⋯ Deficits in visuospatial perception and reasoning not in executive function differentiated freezers from non-freezers. Deficits in visuospatial processing negatively correlated with all SIP freeze metrics, whereas deficits in executive function were only correlated with SIP arrhythmicity, the FOGq total and the duration of freezing episodes. These results suggest that deficits in visuospatial processing to perform a motor task contribute to FOG and that different cognitive deficits may contribute to different aspects of freezing in PD. This is the first study to our knowledge that has compared metrics of freezing to cognitive tasks in the visuospatial and visual reasoning domains.
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Systemic injection of lipopolysaccharide (LPS) induces a robust immune response as well as thermal and mechanical hyperalgesia. Spinal and peripheral glial cells have been implicated as important mediators in this hyperalgesia but the specific contributions of microglia versus astrocytes are not entirely clear. To better define these mechanisms, this study examined the febrile response, nociceptive sensitivity, glial cell reactivity and cytokine production in the dorsal root ganglion (DRG) and spinal cord in rats following systemic treatment with LPS and the effects of minocycline in countering these responses. ⋯ Minocycline suppressed all LPS-induced behavioral effects but not the febrile response. Moreover, minocycline prevented LPS-induced microglia/macrophage activation and cytokine responses in spinal cord and DRG, but did not affect the activation of astrocytes/satellite cells. These data demonstrate that LPS-induced changes in nociceptive sensitivity are likely mediated by activation of microglial cells and/or macrophages in the spinal cord and DRG.
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The mammalian subventricular zone (SVZ) is the largest germinative zone of the adult brain. Progenitor cells generated from the SVZ play important roles during the remyelination process. To determine the functional role of Olig2 in regulating astroglial differentiation in the mouse SVZ, we used the cuprizone mouse model to investigate demyelination. ⋯ Our results indicate that Olig2 may serve as a key regulator during the directional differentiation of progenitor cells after demyelination. The BMP signaling pathway may contribute to the cytoplasmic translocation and altered expression of Olig2 during the remyelination process. These findings provide a better understanding of the mechanisms involved in remyelination.
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Valproic acid (VPA) is a short-chain branched fatty acid with anti-inflammatory, neuro-protective and axon remodeling effects. Here we have studied effects of VPA in gpMBP(68-84)-induced experimental autoimmune encephalomyelitis (EAE). Both preventive (from Day 0 to Day 18) and therapeutic (from Day 7 to Day 18 or from Day 9 to Day 19) VPA (500 mg/kg, intra-gastric) administration to EAE rats once daily greatly reduced the severity and duration of EAE, and suppressed mRNA levels of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-17, matrix metalloproteinase 9 (MMP9), inducible nitric oxide synthase (iNOS) and transcription factor T-bet, but increased levels of IL-4 mRNA in EAE spinal cords. ⋯ VPA treatment altered the cytokine milieu of lymph nodes, modulating the Th profile from Th1 and Th17 to a profile of Th2 and regulatory T cells. In addition, in vitro study showed that VPA inhibited non-specific lymphocyte proliferation in a dose-dependent manner. In summary, our data demonstrated that VPA could suppress systemic and local inflammation to improve outcome of EAE, suggesting that VPA might be a candidate for treatment of multiple sclerosis.