Neuroscience
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Müller cells are not only the main glial cell type in the retina but also latent progenitor/stem cells, which in pathological conditions can transdifferentiate to a neuronal phenotype and regenerate the neurons lost in a mature retina. Several signal transduction pathways can induce the dedifferentiation of mature Müller cells to a progenitor-like state, including that stimulated by glutamate. However, the precise molecular mechanisms by which terminally differentiated cells are initially primed to acquire multipotency remain unclear. ⋯ Importantly, the expression of Müller glia identity genes (i.e., glutamine synthetase; cellular retinaldehyde binding protein, CRALBP) is retained through the process. Dedifferentiated Müller cells held an early neuronal differentiation potential similar to that observed in retinal progenitor-enriched cultures but, contrary to the latter, dedifferentiated Müller cells failed to further differentiate into mature photoreceptor lineages. We speculate that, in spite of the initial triggering of the dedifferentiation pathways, these cells may exhibit a certain degree of epigenetic memory that precludes them from further differentiation.
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Does skill with a difficult task, such as tightrope walking, lead to improved balance through altered movement strategies or through altered weighting of sensory inputs? We approached this question by comparing tandem stance (TS) data between seven tightrope walkers and 12 untrained control subjects collected under different sensory conditions. All subjects performed four TS tasks with eyes open or closed, on a normal firm or foam surface (EON, ECN, EOF, ECF); tightrope walkers were also tested on a tightrope (EOR). Head, upper trunk and pelvis angular velocities were measured with gyroscopes in pitch and roll. ⋯ More time is spent exploring the limits of the base of support with an increased use of fast trunk movements to control balance. Our evidence indicates an increased reliance on neck and pelvis proprioceptive inputs. The similarity of TS on foam to that on the tightrope suggests that the foam tasks are useful for effective training of tightrope walking.
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In the previous report (Sonia Angeline et al., 2012), we showed an altered expression of protective proteins in rotenone-induced Parkinson's disease (PD)-like rat model. This model exhibited a marked attenuation in the expression of parkin, C terminus Hsp70 interacting protein (CHIP) and PARK 7 protein (DJ1) while enhanced levels of caspases and ubiquitin were seen. Herein, we confirmed the neuroprotective role of sesamol and naringenin individually on rotenone-induced rodent model of PD. ⋯ Moreover, improved morphology and survivability of neurons were seen upon sesamol and naringenin treatment in the same rat PD model. Further we confirmed the efficacy of neuroprotective biomolecule administration on muscle from the above PD model and observed the restoration in muscle morphology, elevated level of parkin, DJ1, differential expression of heat shock proteins and reduced cell death. To conclude, for the first time we are demonstrating the comprehensive role of sesamol and naringenin (rotenone-induced PD model) in neuro and myoprotection that would have great clinical significance.
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Synaptic decay and neurodegeneration are hallmarks of Alzheimer's disease that are thought to precede dementia. Recently, we have reported that the first signs of neuritic dystrophy in a new transgenic mouse model of familial Alzheimer's disease (FAD) called the "5xFAD" are axonal dystrophy followed by loss of spines on basal dendrites. The 5xFAD mouse has profound loss of layer 5 neurons by 12months, and these initial structural insults appear between 4 and 6months of age. ⋯ We found these neurons to be structurally and morphologically sound. In parallel, we used in vitro, whole-cell patch clamp electrophysiology of layer 5 pyramidal neurons, from mice aged 8-12weeks, to reveal significant pre- and postsynaptic defects in these cells. Thus our data suggest that layer 5 neurons in the 5xFAD mouse model have synaptic deficits at an early time point, before any overt structural dystrophy, and that such synaptic failure, with co-temporal biochemical changes, may be an early step in neuronal loss.
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Studies involving therapeutic combinations reveal an important benefit in the rehabilitation of neglect patients when compared to single therapies. In light of these observations our present work examines, in healthy individuals, sensorimotor and cognitive after-effects of prism adaptation and neck muscle vibration applied individually or simultaneously. We explored sensorimotor after-effects on visuo-manual open-loop pointing, visual and proprioceptive straight-ahead estimations. ⋯ This is the first demonstration of cognitive after-effects following neck muscle vibration in healthy individuals. The simultaneous application of both methods did not produce significant greater after-effects than prism adaptation alone in both sensorimotor and cognitive tasks. These results are discussed in terms of transfer of sensorimotor plasticity to spatial cognition in healthy individuals.