Neuroscience
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We aimed to evaluate the role of the spinal lymphatic system in spinal cord injury and whether it has an impact on recovery after spinal cord injury. Flow cytometry was used to evaluate the changes in the number of microvesicles after spinal cord injury. Evans blue extravasation was used to evaluate the function of the lymphatic system. ⋯ Microvesicles released after spinal cord injury can enter the thoracic duct and then enter the blood through the lymph around the spine. After ligation of the thoracic duct, it can aggravate the neuropathological manifestations and limb function after spinal cord injury. The potential mechanism may involve nuclear factor-kappa B pathway.
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Glioma is one of the most common and difficult to cure malignant primary tumors of the central nervous system. Long non-coding RNA (lncRNA) has been reported to play important functions in biological processes of many tumors, including glioma. In our study, we aimed to reveal the role and molecular mechanisms of lncRNA COX10-AS1 in regulating the progression of glioma. ⋯ In addition, we uncovered that there existed a regulatory relationship that COX10-AS1 upregulated OCR6 by sponging miR-1-3p in GBM cells, and the following rescue assays demonstrated that both miR-1-3p downregulation and origin recognition complex subunit 6 (ORC6) overexpression rescued cell viability, migration and invasion in the COX10-AS1-deficient GBM cells. Consistently, we also verified that COX10-AS1 promoted tumorigenesis of the GBM cells in vivo through modulating the miR-1-3p/ORC6 axis. On the whole, our findings indicated a novel ceRNA pattern in which COX10-AS1 elevated OCR6 expression via sponging miR-1-3p, therefore boosting tumorigenesis in glioma, and we firstly discussed the underlying mechanisms by which the COX10-AS1/miR-1-3p/ORC6 axis affected the progression of glioma.
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When a musician practices a new song, hitting a correct note sounds pleasant while striking an incorrect note sounds unpleasant. Such reward and punishment feedback has been shown to differentially influence the ability to learn a new motor skill. Recent work has suggested that punishment leads to greater movement variability, which causes greater exploration and faster learning. ⋯ In Experiment 2, we again found that punishment led to significantly less movement variability compared to reward (n = 34). Collectively our results suggest that punishment feedback leads to less movement variability. Future work should investigate whether punishment feedback leads to a greater knowledge of movement variability and or increases the sensitivity of updating motor actions.
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Limb immobilization is known to cause significant decreases in muscle strength and muscle mass as early as two days following the onset of immobilization. However, the decline in strength surpasses the decline in muscle mass, suggesting that factors in addition to muscle loss, such as neuroplasticity, contribute to the decrease in force production. However, little is known regarding immobilization-induced neural changes, although sensorimotor regions seem to be the most affected. ⋯ The results showed changes predominantly involving cerebellar connectivity. For example, the immobilization period caused a decrease in connectivity between the motor cerebellar region of the immobilized arm and the left temporal lobe, and an increase between the same cerebellar region and the supplementary motor area. Overall, changes in connectivity occurred in regions typically associated with error detection and motor learning, suggesting a potential functional reorganization of the brain within 14 days of elbow immobilization.
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The expression levels of SHANK3 are associated with autism spectrum disorder (ASD). The dynamic changes in SHANK3 expression during different stages of brain development may impact the progression of ASD. However, no studies or detailed analyses exploring the upstream mechanisms that regulate SHANK3 expression have been reported. ⋯ Our findings demonstrated that the transcription factor EGR1 regulates SHANK3 expression by binding to the transcription site of the SHANK3 promoter. Although this study did not investigate the pathological phenotypes of human brain organoids or animal model brains with EGR1 deficiency, which could potentially substantiate the findings observed for SHANK3 mutants, our findings provide valuable insights into the relationship between the transcription factor, EGR1, and SHANK3. This study contributes to the molecular understanding of ASD and offers potential foundations for precise targeted therapy.