Spinal cord injury (SCI) represents significant central nervous system trauma and has consistently been a focal point of research in the domain of neural regeneration and repair. Currently, there is n Show more
Spinal cord injury (SCI) represents significant central nervous system trauma and has consistently been a focal point of research in the domain of neural regeneration and repair. Currently, there is no effective treatment available. Various modalities of magnetic stimulation have emerged for recovery from spinal cord injuries; however, the underlying mechanisms remain unclear, significantly hindering the application of magnetic stimulation technologies in treating such injuries. This study aims to elucidate these relevant mechanisms by establishing a simulated closed-loop magnetic stimulation system. In this study, we established a right hemisection model at T8 in mice and administered continuous simulated closed-loop magnetic stimulation targeting the left motor cortex and right L5 nerve root over six weeks. We subsequently utilized a spinal cord dorsal hemisection model to examine regeneration of the corticospinal tract (CST). Motor-evoked potential assessments and calcium imaging techniques were employed to explore neural circuit repair. Additionally, we integrated transcriptomics, proteomics, and metabolomics approaches to investigate related mechanisms. The findings indicate that simulated closed-loop magnetic stimulation effectively restores motor function in the hind limbs, promotes the regeneration of corticospinal tracts in mice with spinal cord injuries, and facilitates the reconstruction of sensorimotor circuits and functions within the spinal cord. Simulated closed-loop magnetic stimulation significantly enhances axonal regeneration of the CST following SCI. This effect may be mediated through the activation of the AMPK-CREB-BDNF signaling pathway, which promotes neurotrophic factor secretion and subsequently induces nerve axon regeneration. This study suggests that simulated closed-loop magnetic stimulation represents a promising therapeutic approach for the treatment for impaired gait following SCI. Show less
Stress exposure, whether acute or chronic, is now recognized to be a determinant of epileptogenic vulnerability. Psychological stress or trauma may not only precipitate seizures but also actively cont Show more
Stress exposure, whether acute or chronic, is now recognized to be a determinant of epileptogenic vulnerability. Psychological stress or trauma may not only precipitate seizures but also actively contribute to the development of epilepsy, a concept that in the clinical setting could be termed "psychoepileptogenesis". Recent evidence from both animal models and clinical studies supports the role of emotional stress in facilitating epileptogenesis, particularly within limbic structures such as the amygdala and hippocampus. In rodent models, chronic stress has been shown to lower seizure thresholds and promote epileptogenesis through mechanisms involving brain-derived neurotrophic factor (BDNF) and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Human studies reinforce these findings: individuals exposed to trauma or suffering from post-traumatic stress disorder (PTSD) exhibit an elevated risk of developing epilepsy, especially temporal lobe epilepsy (TLE), with structural and functional neuroimaging revealing changes in limbic and paralimbic circuits. These converging lines of evidence suggest that psychoepileptogenesis is a plausible, albeit complex, phenomenon. Further research is needed to identify biomarkers of vulnerability and evaluate whether early interventions targeting stress pathways might alter the course of epileptogenesis. Show less