Neuroscience
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There is a large inter-individual variation for umami taste perception. However the neural mechanism for this variability is not well understood. This study investigated brain responses to umami and salty taste among individuals with different umami identification abilities and the effect of repeated oral umami exposure on umami identification and neural processing of taste perceptions. ⋯ In addition, umami identification was significantly improved after umami training for LT. However, it was not reflected in changes in neural activation. The current study shows that attention and association/memory related brain structures play a significant role in the perception of umami taste; and with reference to the results of repeated umami exposure, the presence of very subtle changes regarding the neural processing.
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Intracerebral hemorrhage (ICH) resulting from the rupture of the blood vessels in the brain is associated with significantly higher mortality and morbidity. Clinical studies focused on alleviating the primary injury, hematoma formation and expansion, were largely ineffective, suggesting that secondary injury-induced inflammation and the formation of reactive species also contribute to the overall injury process. In this study, we explored the effects of cofilin knockdown in a mouse model of ICH. ⋯ Cofilin siRNA knocked-down mice had reduced ICH-induced DNA fragmentation, blood-brain barrier disruption and microglial activation, with a concomitant increase in astrocyte activation. Increased expression of pro-survival proteins and decreased markers of oxidative stress were also observed in cofilin siRNA-treated mice possibly due to the reduced levels of cofilin. Our results suggest that cofilin plays a major role in ICH-induced secondary injury, and could become a potential therapeutic target.
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Electrical coupling mediated by connexin36-containing gap junctions that form electrical synapses is known to be prevalent in the central nervous system, but such coupling was long ago reported also to occur between cutaneous sensory fibers. Here, we provide evidence supporting the capability of primary afferent fibers to engage in electrical coupling. In transgenic mice with enhanced green fluorescent protein (eGFP) serving as a reporter for connexin36 expression, immunofluorescence labeling of eGFP was found in subpopulations of neurons in lumbar dorsal root and trigeminal sensory ganglia, and in fibers within peripheral nerves and tissues. ⋯ Expression of eGFP was also found in various proportions of sensory ganglion neurons containing transient receptor potential (TRP) channels, including TRPV1 and TRPM8. Ganglion cells labeled for isolectin B4 and tyrosine hydroxylase displayed very little co-localization with eGFP. Our results suggest that previously observed electrical coupling between peripheral sensory fibers occurs via electrical synapses formed by Cx36-containing gap junctions, and that some degree of selectivity in the extent of electrical coupling may occur between fibers belonging to subpopulations of sensory neurons identified according to their sensory modality responsiveness.
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Recent studies investigating neural correlates of human thirst have identified various subcortical and telencephalic brain areas. The experience of thirst represents a homeostatic emotion and a state that slowly evolves over time. Therefore, the present study aims at systematically examining cerebral perfusion during the parametric progression of thirst. ⋯ However, significant differences across all four thirst stages (including the moderate thirst level), were exclusively found in the posterior insular cortex. The subjective thirst ratings over the different thirst stages, however, were associated with perfusion differences in the right anterior insula. These findings add to our understanding of the insular cortex as a key player in human thirst - both on the level of physiological dehydration and the level of the subjective thirst experience.
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Ascend to high altitude results in a drastic change in the environmental conditions an individual is exposed to. As the altitude increases there is a decrease in partial pressure of oxygen leading to a unique condition known as hypobaric hypoxia (HH). Brain is highly vulnerable to hypoxia and it has been well established that hypobaric hypoxia leads to neurodegeneration in different brain regions. ⋯ The study also explored the role of microglia and A1 astrocyte interplay in HH-induced neurodegeneration and demyelination. This study explores the shift in role of glial cell toward neurodegeneration under chronic hypobaric hypoxia stress. Chronic stress results in glial activation which leads to neuroinflammation a plausible factor in HH-induced neurodegeneration.