Neuroscience
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Randomized Controlled Trial
Early exercise after intracerebral hemorrhage inhibits inflammation and promotes neuroprotection in the sensorimotor cortex in rats.
The present study examined the effect of early exercise on brain damage and recovery of motor function following intracerebral hemorrhage (ICH) in rats. Subjects were randomly assigned to no training after ICH (ICH), no training after sham surgery (SHAM), early treadmill exercise after ICH (ICH + ET), and late treadmill exercise after ICH (ICH + LT) groups. The ICH + ET and ICH + LT groups were trained for seven consecutive days starting on day 2 and day 9 after surgery, respectively. ⋯ Expression of IL-1b mRNA was significantly lower in the ICH + ET group than that in the ICH group. Collectively, these results suggest that early treadmill exercise after ICH promotes recovery of sensorimotor function by preventing neuronal death and ensuing cortical atrophy and by preserving dendritic structure compared with late treadmill exercise and no exercise. Early exercise may prevent neurodegeneration and functional loss by inhibiting neuroinflammation.
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The complexity of brain activity has recently been investigated using the Hurst exponent (H), which describes the extent to which functional magnetic resonance imaging (fMRI) blood oxygen-level dependent (BOLD) activity is simple vs. complex. For example, research has demonstrated that fMRI activity is more complex before than after consumption of alcohol and during task than resting state. The measurement of H in fMRI is a novel method that requires the investigation of additional factors contributing to complexity. ⋯ Multiple regression analyses demonstrated that eigenvector centrality was the most robust predictor of complexity, whereby greater centrality was associated with increased complexity (lower H). Regions known to be highly connected, including the thalamus and hippocampus, notably were among the highest in centrality and complexity. This research has led to a greater understanding of how brain region characteristics such as DTI centrality relate to the novel Hurst exponent approach for assessing brain activity complexity, and implications for future research that employ these measures are discussed.
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Binge drinking is a common pattern of adolescent alcohol consumption characterized by a high alcohol intake within a short period of time; which may seriously affect brain function, triggering in some cases an addictive behavior. Current evidence indicates that alcohol addictive conduct is related to the impairment of the Melanocortin System (MCS). This system participates in the regulation of food intake and promotes anti-inflammatory response in the brain. ⋯ Additionally, MC4R activation prevented mitochondrial potential loss and increased mitochondrial mass that were significantly reduced by binge ethanol protocol. Finally, RO27-3225 treatment increased ATP production and mitochondrial respiratory complex expression in adolescent rats exposed to ethanol. Altogether, these findings show that activation of the MCS pathway through MC4R prevents these negative effects of binge ethanol protocol, suggesting a possible role of the MCS in the reduction of the neurotoxic effects induced by alcohol intoxication in adolescents.
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Human visual function degrades with age. Previous studies of visual perception have shown that aged people have worse performance in the coding of orientation information. However, the neuronal mechanism still remains elusive. ⋯ Further investigation of neuronal correlation showed higher noise and signal correlations in aging monkeys than that in young monkeys. These correlation changes predicted a detrimental effect on the efficiency of population coding of orientation information. Taken together, our results suggest that the information coding efficiency of orientation information is impaired during aging and might account for the degradation of performance in human fine orientation discrimination task.
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The miRNA miR-124 has been reported to be a promising target for the repair of spinal cord injury (SCI), which is a devastating neurological condition. This study aimed to investigate the underlying molecular mechanisms of miR-124-mediated SCI repair. We established miR-124 SCI model rats and further treated them with agomiR-124 for 14 days. ⋯ In addition, we noted that Tal1 is a potential target gene of miR-124, and that a low level of this gene promoted the proliferation of neuronal precursor cells and inhibited their differentiation. In conclusion, miR-124 was able to mediate SCI repair by altering the expression of various mRNAs in rats. The miR-124/Tal1 axis may participate in the treatment of SCI by agomiR-124 by repopulating neural stem cells.