Neuroscience
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Chronic psychosocial stress modulates brain antioxidant systems and causes neuroinflammation that plays a role in the pathophysiology of depression. Although the antidepressant fluoxetine (FLX) represents the first-line treatment for depression and the atypical antipsychotic clozapine (CLZ) is considered as a second-line treatment for psychotic disorders, the downstream mechanisms of action of these treatments, beyond serotonergic or dopaminergic signaling, remain elusive. We examined behavioral changes, glutathione (GSH)-dependent defense and levels of proinflammatory mediators in the prefrontal cortex (PFC) of adult male Wistar rats exposed to 21days of chronic social isolation (CSIS). ⋯ In conclusion, prefrontal cortical GSH depletion and the proinflammatory response underlying depressive- and anxiety-like states induced by CSIS were prevented by FLX. The protective effect of CLZ, which was equally effective as FLX on the behavioral level, was limited to proinflammatory components. Hence, different mechanisms underlie the protective effects of these two drugs in CSIS rats.
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Simvastatin ameliorates memory impairment and neurotoxicity in streptozotocin-induced diabetic mice.
Diabetes comes with an additional burden of moderate to severe hyperlipidemia, but little is known about the effects of lipid-lowering therapy on diabetic complications such as diabetes-associated cognitive decline. Herein we investigated the effects of statins on memory impairment and neurotoxicity in streptozotocin-induced diabetic mice. Our data indicated that oral administration of simvastatin at 10 or 20mg/kg for 4weeks significantly ameliorated diabetes-associated memory impairment reflected by performance better in the Morris water maze and Y-maze tests. ⋯ Moreover, simvastatin pronouncedly attenuated amyloidogenesis by decreasing amyloid-β, amyloid precursor protein (APP) and beta-site APP cleaving enzyme-1. As expected, treated with simvastatin, the diabetic mice exhibited significant improvement of hyperlipidemia rather than hyperglycemia. Our findings disclosed novel therapeutic potential of simvastatin for the diabetes-associated cognitive impairment.
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It is still unclear if muscle synergies reflect neural strategies or mirror the underlying mechanical constraints. Therefore, this study aimed to verify the consistency of muscle groupings between the synergies based on the linear envelope (LE) of muscle activities and those incorporating the time-frequency (TF) features of the electromyographic (EMG) signals. Twelve healthy participants performed six 20-m walking trials at a comfort and fast self-selected speed, while the activity of eleven lower limb muscles was recorded by means of surface EMG. ⋯ When accounting the reconstruction level of the initial dataset, a new TF synergy emerged. This new synergy dissociated the activity of the rectus femoris from those of the vastii muscles (synergy #1) and from the one of the tensor fascia latae (synergy #5). Overall, extracting TF muscle synergies supports the neural origin of muscle synergies and provides an opportunity to distinguish between prescriptive and descriptive muscle synergies.
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Rapamycin (RAPA), an inhibitor of mammalian target of rapamycin (mTOR), exhibits a high neuroprotective action against neurodegenerative diseases in mouse models. Since neuroinflammation has been shown to be involved in Alzheimer's disease (AD) development and progression, the aim of this study was to examine the anti-inflammatory role of RAPA in AD in vivo and in vitro, and investigate the underlying mechanisms. ⋯ Moreover, RAPA disrupted Aβ25-35-induced nuclear translocation of mTOR and NF-κB. Our findings indicate that RAPA inhibits Aβ25-35- or LPS-induced neuronal inflammation through suppressing mTOR signaling and reducing nuclear import of NF-κB.