Neuroscience
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Ischemic stroke remains the third leading cause of death and leading cause of adult disability worldwide. A key event in the pathophysiology of stroke is the anoxic depolarization (AD) of neurons in the ischemic core. Previous studies have established that both the latency to AD and the time spent in AD prior to re-oxygenation are predictors of neuronal death. ⋯ Experiments using slices with fields Cornu ammonis 3 (CA3) and Cornu ammonis 1 (CA1) disconnected showed that AD latency is longer in CA1 than in CA3; however, the early AD in CA3 is propagated to CA1 in intact slices. Finally, AD latency in CA1 was found to be longer in slices from female mice than in those from age-matched male mice. The results have implications for stroke prevention and for understanding brain adaptations in hypoxia-tolerant animals.
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As a textbook manifestation of an aggressive attitude, hostility can pose a serious threat to both an individual's life and the security of society at large. Past evidence suggests that some anxiety-related traits may be more prone to giving rise to hostility. However, many aspects of hostility, such as, determining the susceptible temperament for hostility, the neural basis of hostility, and the underlying mechanisms through which having a susceptible temperament generates hostility in a healthy brain, remain unclear. ⋯ Finally, we used a mediation analysis to explore the tripartite relationship between vulnerability temperament, the fractional anisotropy (FA) value of the white matter, and hostility. Our results suggest that a harm avoidance temperament may be susceptible to hostility and that the cingulum may be a key white matter region responsible for hostility. Based on these results, we developed a temperament-brain-attitude pathway showing how harm avoidance temperament could affect the brain and ultimately lead to hostility.
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Human behaviour amazes with extraordinary flexibility and the underlying neural mechanisms have often been studied using task switching. Despite extensive research, the relative importance of "cognitive" and "motor" aspects during switching is unclear. In the current study we examine this question combining EEG analysis techniques and source localization to examine whether the selection of the response, or processes during the execution of the response, contribute most to switching effects. ⋯ On a functional neuroanatomical level, these modulations in motor processes showed a clear temporal sequence in that motor codes are processed primarily in superior parietal regions (Brodman area 7) and only then in premotor regions (Brodman area 6). The observed modulations may reflect motor reprogramming processes. The study shows how EEG signal analysis in combination with brain mapping methods can inform debates on theories of human cognitive flexibility.
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Caveolin-1 (Cav-1) is a constitutive structural protein of caveolae in the plasma membrane. It plays an important role in maintaining blood brain barrier (BBB) integrity. In this study, we identified that miR-103-3p, a hypoxia-responsive miRNA, could interact with Cav-1. ⋯ Pre-SAH intracerebroventricularly injection of miR-103-3p antagomir relieved Cav-1 loss, sequentially reduced BBB permeability and improved neurological function. Finally, we demonstrated that the salutary effects of miR-103-3p antagomir were abolished in Cav-1 knock-out mice, suggesting that Cav-1 was required for the miR-103-3p inhibition-induced neurovascular protection. Taken together, our findings suggest that the inhibition of miR-103-3p could exert neuroprotective effects through preservation of Cav-1 and BBB integrity, making miR-103-3p a novel therapeutic target for SAH.
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By the effort to identify candidate signaling molecules important for the formation of robust circadian rhythms in the suprachiasmatic nucleus (SCN), the mammalian circadian center, here we characterize the role of α2δ proteins, synaptic molecules initially identified as an auxiliary subunit of the voltage dependent calcium channel, in circadian rhythm formation. In situ hybridization study demonstrated that type 3 α2δ gene (α2δ3) was strongly expressed in the SCN. ⋯ Cultured SCN slices from Per1-luc transgenic Cacna2d3-/- mice revealed reduced synchrony of Per1-luc gene expression rhythms among SCN neurons. These findings suggest that α2δ3 is essential for synchronized cellular oscillations in the SCN and thereby contributes to enhancing the sustainability of circadian rhythms in behavior.