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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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.
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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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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.