Neuroscience
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Memories already consolidated when reactivated return to a labile state and can be modified, this process is known as reconsolidation. It is known the Wnt signaling pathways can modulate hippocampal synaptic plasticity as well as learning and memory. Yet, Wnt signaling pathways interact with NMDA (N-methyl-D-aspartate) receptors. ⋯ Moreover, the impairment induced by DKK1 was blocked by the administration of the agonist of the NMDA receptors glycine site, D-Serine, immediately and 2 h after reactivation session. We found that hippocampal canonical Wnt/β-catenin is necessary to the reconsolidation of CFC memory at least two hours after reactivation, while non-canonical Wnt/Ca2+ signaling pathway is not involved in this process and, that there is a link between Wnt/β-catenin signaling pathway and NMDA receptors. In view of this, this study provides new evidence regarding the neural mechanisms underlying contextual fear memory reconsolidation and contributes to provide a new possible target for the treatment of fear related disorders.
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The frontoparietal network (FPN) and cingulo-opercular network (CON) may exert top-down regulation corresponding to the central executive system (CES) in working memory (WM); however, contributions and regulatory mechanisms remain unclear. We examined network interaction mechanisms underpinning the CES by depicting CON- and FPN-mediated whole-brain information flow in WM. We used datasets from participants performing verbal and spatial working memory tasks, divided into encoding, maintenance, and probe stages. ⋯ Task-level output was slightly stronger for the CON. CON → FPN, CON → DMN, visual areas → CON, and visual areas → FPN showed consistent effects. The CON and FPN might together underlie the CES's neural basis and achieve top-down regulation through information interaction with other large-scale functional networks, and the CON may be a higher-level regulatory core in WM.
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Vitamin C (VC) is a key antioxidant of the Central Nervous System (CNS) and SLC23A2 (SVCT2) is the only transporter that actively transports VC into the brain. While the existing animal models of VC deficiency are in the whole body, the essential role of VC in brain development remains elusive. ⋯ On the other hand, the levels of Glutathione, Reduced (GSH), myeloperoxidase (MDA), 8-isoprostane, tumor necrosis factor-α (TNF-α) and interleukin-6(IL-6) were significantly increased, but the levels of VC in brain tissue of the model group were decreased in Cre;svct2 f/f mice brain tissues, indicating the protective effect of VC against oxidative stress and inflammation during pregnancy. Thus, the conditional knockout of the SLC23A2 gene in the brain of mouse was successfully established by the CRISPR/Cas9 technology in our study, providing an effective animal model for studying the role of VC in fetal brain development.
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The human brain presents a heavily connected complex system. From a relatively fixed anatomy, it can enable a vast repertoire of functions. One important brain function is the process of natural sleep, which alters consciousness and voluntary muscle activity. ⋯ The results demonstrated that the delta-alpha coupling function was increasing gradually from Awake to NREM3 (non-rapid eye movement), but only during NREM2 and NREM3 deep sleep it was significant in respect of surrogate data testing. The analysis on the spatially distributed connections showed that this significance is strong only for within the single electrode region and in the front-to-back direction. The presented methodological framework is for the whole-night sleep recordings, but it also carries general implications for other global neural states.
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Ginkgo biloba L. leaf extract (GBE) has been added in many commercial herbal formulations such as EGb 761 and Shuxuening Injection to treat cardiovascular diseases and stroke worldwide. However, the comprehensive effects of GBE on cerebral ischemia remained unclear. Using a novel GBE (nGBE), which consists of all the compounds of traditional (t)GBE and one new compound, pinitol, we investigated its effect on inflammation, white matter integrity, and long-term neurological function in an experimental stroke model. ⋯ In vitro analyses showed that nGBE treatment reduced the production of IL-1β and TNFα in primary microglia. Administration of nGBE also decreased the SMI-32/MBP ratio and enhanced myelin integrity, thus exhibiting improved white matter integrity at 28 days post stroke. These findings demonstrate that nGBE protects against cerebral ischemia by inhibiting microglia-related inflammation and promoting white matter repair, suggesting that nGBE is a promising therapeutic strategy for long-term recovery after stroke.