Neuroscience
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Traumatic brain injury (TBI) induces significant neuroinflammation, primarily driven by microglia. Neonatal microglia (NMG) may have therapeutic potential by modulating the inflammatory response of damaged adult microglia (AMG). This study investigates the influence of NMG on AMG function through extracellular matrix (ECM) remodeling and the formation of tunneling nanotubes (TnTs), with a focus on the role of Serpina3n. ⋯ Inhibition of Serpina3n in NMG increased pro-inflammatory markers and decreased TnTs formation proteins, whereas overexpression of M-sec in AMG counteracted these effects. This highlights the importance of TnTs in maintaining microglial function and promoting an anti-inflammatory environment. In conclusion, NMG improve the function of damaged AMG by modulating ECM remodeling and promoting TnTs formation through the action of Serpina3n.
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Sevoflurane impairs learning and memory of the developing brain. However, strategies to mitigate these detrimental effects have been scarce. Herein, we investigated whether tetramethylpyrazine pretreatment could alleviate the impairment of learning and memory and its underlying mechanism in sevoflurane-exposed neonatal rats. ⋯ It was found that neonatal exposure of sevoflurane impaired learning and memory, increased neuronal apoptosis, altered the morphology of dendritic spines, upregulated the expressions of NMDAR2A and PSD95, and induced LTP deficits. Pretreatment with tetramethylpyrazine not only alleviated impairment of learning and memory, but also improved sevoflurane-induced changes in neuronal damage, dendritic spine morphology, NMDAR2A and PSD95 expressions, as well as LTP. These findings indicated that pretreatment with tetramethylpyrazine alleviated the impairment of learning and memory induced by sevoflurane through improvement of hippocampal synaptic plasticity in neonatal rats.
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Complexity of neuronal firing patterns may serve as an indicator of sensory information processing across different states of consciousness. Recent studies have shown that spontaneous changes in brain states can occur during general anesthesia, which may influence neuronal complexity and the state of consciousness. In this study, we investigated how the firing patterns of cortical neurons, both at rest and during visual stimulation, are affected by spontaneously changing brain states under varying levels of anesthesia. ⋯ However, this was contradicted by the observation of low neuronal complexity in both spontaneous and stimulus-related spike activity, which more closely aligns with unconsciousness. Our findings reveal that transient neuronal states with distinct spiking patterns can emerge in visual cortex at constant anesthetic concentrations. The reduced complexity in states associated with deep anesthesia likely indicates a disruption of conscious sensory information processing.
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Ginsenoside Rg1 (Rg1) has been shown to treat a variety of human diseases, including Alzheimer's disease (AD). However, its mechanism in AD needs further investigation. Microglial cells (BV2) were treated with Aβ1-42 to induce AD cell models. ⋯ GATA4 interacted with PDE4A, and GATA4 facilitated Aβ1-42-induced BV2 cell injury by increasing PDE4A expression. Besides, GATA4 knockdown reduced PDE4A protein expression and inactivated PI3K/AKT axis, while these effects were abolished by PDE4A overexpression. In conclusion, our data suggested that Ginsenoside Rg1 inhibited microglial cell apoptosis and inflammation to attenuate AD progression by regulating the GATA4/PDE4A/PI3K/AKT axis.
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Similar to other brain regions, the neurons in the lateral septum (LS) are of heterogeneous populations. However, their resting membrane potential (RMP) on average is not too far apart. Cells were characterized based on biological markers by using brain slices, as under these in vitro conditions, neurons retain their morphologies. ⋯ The type III AP is selectively triggered by Ca2+ in GAD and SOM-positive neurons. Conclusions are supported by established pharmacologic tools, nimodipine, TTX, and ZD7288, a selective HCN channel antagonist. Collectively, these observations revitalize our knowledge from pioneering studies with regard to the brain of mammals in general and septal structures in particular.