Neuroscience
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In 2017, the Food and Drug Administration published a safety recommendation to limit the exposure to general anesthesia as much as possible below the age of three. Indeed, several preclinical and clinical studies have questioned the possible toxicity of general anesthesia on the developing brain. Since then, recent clinical studies tried to mitigate this alarming issue. ⋯ Only stronger translational research will allow scientists to provide concrete answers to this public health issue. In this review, we will provide and discuss the more recent data in this field, including the point of view of preclinical researchers, neuropsychologists and pediatric anesthesiologists. Through translational research, preclinical researchers have more than ever a role to play to better understand and identify long-term effects of general anesthesia for pediatric surgery on brain development in order to minimize it.
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Glutamate (Glu) is known as the main excitatory neurotransmitter in the central nervous system. It can trigger a series of processes ranging from synaptic plasticity to neurophysiological regulation. To carry out its functions, Glu acts via interaction with its cognate receptors, which are ligand-dependent. ⋯ Therefore, the aim of this review was to summarize the current knowledge regarding iGluRs, while describing their structures and molecular mechanisms of action, including their role in excitotoxicity, as well as the current strategies to reduce excitotoxic damage. Particularly, strategies mediated by prolactin, a somatotropin family-related hormone that displays a significant neuroprotective effect against both Glu and kainic acid-induced excitotoxicity in the hippocampus, are described. Finally, the role of prolactin as a possible molecule in the treatment of excitotoxicity in neurological diseases is discussed.
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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.