Neuroscience
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Changes in inhibition following traumatic brain injury (TBI) appear to be one of the major factors that contribute to excitation:inhibition imbalance. Neuron pathology, interneurons in particular evolves from minutes to weeks post injury and follows a complex time course. Previously, we showed that in the long-term in diffuse TBI (dTBI), there was select reduction of specific dendrite-targeting neurons in sensory cortex and hippocampus while in motor cortex there was up-regulation of specific dendrite-targeting neurons. ⋯ However, DG of hippocampus now showed reduction of dendrite-targeting inhibitory neurons. Finally, with respect to motor cortex, there was an upregulation of dendrite-targeting interneurons in the supragranular layers at 24 h returning to normal levels by 2 weeks. Overall, our findings reconfirm that dendritic inhibition is particularly susceptible to brain trauma, but also show that there are complex brain-area-specific changes in inhibitory neuronal numbers and in compensatory changes, rather than a simple monotonic progression of changes post-dTBI.
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The purpose of this study was to determine the response, in rat, to chronic physical activity in small and large DRG neurons. Rats were cage-confined or underwent 16-18 weeks of daily increased activity, via 2 h of treadmill running per day or free access to voluntary exercise wheels, following which small (≤30 µm) and large (≥40 µm) diameter DRG neurons were harvested by laser capture microdissection from flash-frozen lumbar DRGs. Relative mRNA levels were determined using real-time polymerase chain reaction. ⋯ In large DRG neurons, voluntary wheel exercise decreased the expression for 5HT1D receptors, whereas both treadmill and voluntary wheel exercise decreased the expression of mRNA for TrkC receptors. DRG neurons show slightly more changes in gene expression after voluntary exercise compared to the treadmill exercise group. Small and large lumbar sensory neurons are responsive to chronically increased neuromuscular activity by changing the expression of genes, the products of which could potentially change the sensory processing of nociceptors and proprioceptors, which could in turn alter functions such as pain transmission and locomotor coordination.
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Peripheral immune activation could cause neuroinflammation, leading to a series of central nervous system (CNS) disorders, such as spatial learning and memory dysfunction. However, its pathogenic mechanism and therapeutic strategies are not yet determined. The present study aimed to investigate the therapeutic effects of sulforaphane (SFN) on lipopolysaccharide (LPS)-induced spatial learning and memory dysfunction, and tried to elucidate its relationship with the role of hippocampal brain-derived neurotrophic factor (BDNF)-mammalian target of rapamycin (mTOR) signaling pathway. ⋯ In addition, hippocampal levels of inflammatory cytokines, synaptic proteins, BDNF-tropomyosin receptor kinase B (TrkB) and mTOR signaling pathways were altered in the processes of LPS-induced cognitive dysfunction and SFN's therapeutic effects. Furthermore, we found that ANA-12 (a TrkB inhibitor) or rapamycin (a mTOR inhibitor) could block the beneficial effects of SFN on LPS-induced cognitive dysfunction, and that hippocampal levels of synaptic proteins, BDNF-TrkB and mTOR signaling pathways were also notably changed. In conclusion, the results of the present study suggest that SFN could elicit improving effects on LPS-induced spatial learning and memory dysfunction, which is likely related to the regulation of hippocampal BDNF-mTOR signaling pathway.
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The aim of this cross-sectional study was to determine the associations of objectively assessed habitual physical activity and physical performance with brain plasticity outcomes and brain-derived neurotrophic factor (BDNF) levels in cognitively healthy older adults. Physical performance was analyzed based on cardiopulmonary exercise-testing data and accelerometer-based physical activity was analyzed as total activity counts, sedentary time, light physical activity and moderate to vigorous physical activity. Brain plasticity outcomes included magnetic resonance spectroscopy (MRS)-based markers, quantitative imaging-based hippocampal volume and BDNF serum levels. ⋯ In this study these associations were not mediated significantly by physical performance. Overall physical activity and exceeding current moderate to vigorous physical activity recommendations were positively associated with BDNF. Sedentary behavior, however, seems to be negatively related to neurotrophic factor bioavailability in the elderly.
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Incorporation of a tool into the body schema is well established. Here, we assessed whether visual signals originating from the tool provide relevant cues for the perception of arm movements, as would signals originating from the arm holding it. Kinesthetic illusions were investigated by passively moving one arm (via a robotized manipulandum) and therefore the tool (a rake), using the mirror paradigm, with the reflected part being limited to the tool, the arm, or both. ⋯ Results showed that mirror vision of the moving tool was not sufficient for mirror illusions to occur, the same tool in the two hands being an essential condition. Finally, in Experiment 3, we showed that neither prior practice nor active tool use was necessary for the tool mirror illusion to occur. Altogether, these results demonstrate that the visual cues originating from the held-tool are integrated for sensing arm movement.