Neuroscience
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Clinical and preclinical studies suggest that early life stress can increase the risk of developing ethanol use disorder later in life. Although the endocannabinoid (eCB) system plays a role in stress-related behaviors and ethanol consumption, it remains unclear whether the eCB system is affected in response to a combination of both factors. ⋯ In Experiment 2, during a two-bottle free choice paradigm, we found that MS increased mice preference for high ethanol concentrations (15 % and 20 %) but not lower ethanol concentrations (5 % and 10 %). Except for Mgll gene expression in the dorsal striatum (DS) in Experiment 2, no statistically significant effects of MS were observed regarding neuronal activation on the prefrontal cortex, DS, globus pallidus, and substantia nigra following a binge operant ethanol self-administration session (Experiment 1) or the eCB system molecules (Cnr1 and Faah gene expression) in the DS (Experiment 2).
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Postoperative neurocognitive disorder (PND) is a prevalent complication following surgery and anesthesia, characterized by progressive cognitive decline. The precise etiology of PND remains unknown, and effective targeted therapeutic strategies are lacking. Transcranial near-infrared light (tNIRL) has shown potential benefits for cognitive dysfunction diseases, but its effect on PND remains unclear. ⋯ Furthermore, tNIRL increased the expression of oligodendrocyte transcription factor 2 (OLIG2) and myelin basic protein (MBP), promoting remyelination while enhancing synaptic function-associated proteins such as synaptophysin (SYP) and postsynaptic density protein 95 (PSD95). Further investigation revealed that tNIRL may activate the AKT1/mTOR pathway to facilitate remyelination in PND mice. These findings indicate that tNIRL is a novel non-invasive therapeutic approach for treating PND.
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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.