Neuroscience
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As an adult-onset neurodegenerative disease, amyotrophic lateral sclerosis (ALS) results in progressive muscular atrophy and paralysis. However, the mechanism of ALS has not yet been elucidated, and no cure has been found. Research has revealed that a mutation of the Cu/Zn superoxide dismutase (SOD1) gene is linked to familial ALS and that potential sex discrepancies exist in ALS incidence. ⋯ This protective effect occurred through anti-apoptotic pathways related to estrogen receptor-alpha (ER-α) activation. Meanwhile, knockdown of aromatase with Cyp19a1 ShRNA plasmid transfection reduced cell proliferation, increased cell damage, promoted apoptosis, and decreased ER-α expression in hSOD1-G93A cells, and the induced apoptotic effects could be reversed by estradiol (E2). In brief, the results of our study suggest that aromatase plays a neuroprotective role against apoptosis in hSOD1-G93A cells by activating ER-α and may become a new intervention target for ALS treatment.
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We study the transition in the functional networks that characterize the human brains' conscious-state to an unconscious subliminal state of perception by using k-core percolation. We find that the most inner core (i.e., the most connected kernel) of the conscious-state functional network corresponds to areas which remain functionally active when the brain transitions from the conscious-state to the subliminal-state. ⋯ Thus, the inner core and most robust component of the conscious brain corresponds to the unconscious subliminal state. This finding imposes constraints to theoretical models of consciousness, in that the location of the core of the functional brain network is in the unconscious part of the brain rather than in the conscious state as previously thought.
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Parkinson disease (PD) is a leading neurodegenerative disease, with multifaceted interacting mechanisms. The Thy1-aSyn mouse model of PD exhibits many features of PD patients, including sensorimotor and olfactory dysfunction and protein aggregation. Here, we tested the hypothesis that the dipeptide carnosine, which has anti-aggregating and metal-chelating properties, would provide beneficial effects on the motor and olfactory deficits observed in Thy1-aSyn mice. ⋯ In contrast, intranasal carnosine prevented the normal decline in gait function seen in the challenging beam test in the Thy1-aSyn mice. Moreover, carnosine-treated Thy1-aSyn mice exhibited decreased aSyn immunostaining in the olfactory epithelium compared to vehicle-treated Thy1-aSyn mice, and the carnosine transporter Pept2 was immunolocalized to the apical surface of the olfactory epithelium. These findings demonstrate that intranasal carnosine shows promise in slowing the progression of motor deficits and aSyn deposition in PD.
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The present study investigated how pain appraisals from other individuals modulated self-pain anticipation and perception. Appraisals of pain intensity from 10 other individuals were presented before the participants received identical electrical pain stimulation themselves. In reality, the presented other's pain appraisals, with either low or high in mean and variance, were generated by the experimenter, and were randomly paired with the subsequent electrical stimulation at either low or high intensity. ⋯ In contrast, when the mean was high, the higher variance enhanced sensorimotor α-oscillations and suppressed subsequent pain perception. These results demonstrated that others' pain appraisals can modulate both of the anticipation and perception of first-hand pain. It also suggested that the top-down modulation of others' pain appraisals on pain perception could be partially driven by the different brain states during the anticipation stage, as captured by the prestimulus sensorimotor α-oscillations.
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Insulin Modulates Excitatory Synaptic Transmission and Synaptic Plasticity in the Mouse Hippocampus.
The administration of exogenous insulin into the hippocampus has the potential to enhance cognitive function and exert other beneficial effects. Elucidating the neurobiological substrates of insulin action and its underlying physiological mechanisms may further improve treatment efficacy. Previous work has shown that insulin affects synaptic plasticity, however there are discrepancies and contradictory conclusions between studies. ⋯ Moreover, a broad spectrum protein kinase C blocker, cannabinoid receptor type 1 activator, or a high glucose concentration inhibited fEPSPs per se, and disturbed insulin's effect on fEPSP. Insulin also caused depotentiation during LTP expression and triggered depression during LTD recovery. Given the essential roles of dynamic synaptic transmission and plasticity in learning and memory, our data provide more evidence that insulin application may actively modulate hippocampal-dependent cognitive events.