Edvardsenconnor8157

Furthermore, we transplanted the porcine decellularized optic nerve containing neurotrophin-3-overexpressing Schwann cells in a rat model of T10 spinal cord defect in vivo. Four weeks later, the regenerating axons grew straight, the myelin sheath in the injured/transplanted area recovered its structure, and simultaneously, the number of inflammatory cells and the expression of chondroitin sulfate proteoglycans were reduced. Together, these findings suggest that porcine decellularized optic nerve loaded with Schwann cells overexpressing neurotrophin-3 promotes the directional growth of regenerating spinal cord axons as well as myelin regeneration. All procedures involving animals were conducted in accordance with the ethical standards of the Institutional Animal Care and Use Committee of Sun Yat-sen University (approval No. SYSU-IACUC-2019-B034) on February 28, 2019.Somatosensory evoked potentials (SEPs) have been widely used to assess neurological function in clinical practice. A good understanding of the association between SEP signals and neurological function is helpful for precise diagnosis of impairment location. Previous studies on SEPs have been reported in animal models. However, few studies have reported the relationships between SEP waveforms in animals and those in humans. In this study, we collected normal SEP waveforms and decomposed them into specific time-frequency components (TFCs). Our results showed three stable TFC distribution regions in intact goats and rats and in humans. After we induced spinal cord injury in the animal models, a greater number of small TFC distribution regions were observed in the injured goat and rat groups than in the normal group. Moreover, there were significant correlations (P less then 0.05) and linear relationships between the main SEP TFCs of the human group and those of the goat and rat groups. A stable TFC distribution of SEP components was observed in the human, goat and rat groups, and the TFC distribution modes were similar between the three groups. Results in various animal models in this study could be translated to future clinical studies based on SEP TFC analysis. Human studies were approved by the Institutional Review Board of the University of Hong Kong/Hospital Authority Hong Kong West Cluster (approval No. UM 05-312 T/975) on December 5, 2005. Rat experiments were approved by the Committee on the Use of Live Animals in Teaching and Research of Li Ka Shing Faculty of Medicine of the University of Hong Kong (approval No. CULART 2912-12) on January 28, 2013. Goat experiments were approved by the Animal Ethics Committee of Affiliated Hospital of Guangdong Medical University (approval No. GDY2002132) on March 5, 2018.The globus pallidus is the relay nucleus of the basal ganglia, and changes in its electrical activity can cause motor impairment. Apelin-13 is widely distributed in the central and peripheral nervous systems. It has been demonstrated that apelin-13 plays important roles in the regulation of blood pressure and other non-motor functions. However, its role in motor function has rarely been reported. In the present study, apelin-13 (10 μM/100 μM) was injected into the globus pallidus of rats. The results showed that apelin-13 increased the spontaneous discharges in the majority of pallidal neurons. However, an apelin-13-induced inhibitory effect on the firing rate was also observed in a few pallidal neurons. In postural tests, after the systemic administration of haloperidol, unilateral pallidal injection of apelin-13 caused a contralateral deflection. Together, these findings suggest that apelin-13 regulates the electrical activity of pallidal neurons and thus participates in central motor control in rats. The study was approved by the Animal Ethics Committee of Qingdao University (approval No. 20200615Wistar0451003020) on June 15, 2020.Our previous study has confirmed that astrocytes overexpressing neurogenic differentiation factor 1 (NEUROD1) in the spinal cord can be reprogrammed into neurons under in vivo conditions. However, whether they can also be reprogrammed into neurons under in vitro conditions remains unclear, and the mechanisms of programmed conversion from astrocytes to neurons have not yet been clarified. In the present study, we prepared reactive astrocytes from newborn rat spinal cord astrocytes using the scratch method and infected them with lentivirus carrying NEUROD1. selleck chemical The results showed that NEUROD1 overexpression reprogrammed the cultured reactive astrocytes into neurons in vitro with an efficiency of 13.4%. Using proteomic and bioinformatic analyses, 1952 proteins were identified, of which 92 were differentially expressed. Among these proteins, 11 were identified as candidate proteins in the process of reprogramming based on their biological functions and fold-changes in the bioinformatic analysis. Furthermore, western blot assay revealed that casein kinase II subunit alpha (CSNK2A2) and pinin (PNN) expression in NEUROD1-overexpressing reactive astrocytes was significantly increased, suggesting that NEUROD1 can directly reprogram spinal cord-derived reactive astrocytes into neurons in vitro, and that the NEUROD1-CSNK2A2-PNN pathway is involved in this process. This study was approved by the Animal Ethics Committee of Fujian Medical University, China (approval No. 2016-05) on April 18, 2016.Tinnitus can be described as the conscious perception of sound without external stimulation, and it is often accompanied by anxiety, depression, and insomnia. Current clinical treatments for tinnitus are ineffective. Although recent studies have indicated that the caudate-putamen nucleus may be a sensory gating area involved in noise elimination in tinnitus, the underlying mechanisms of this disorder are yet to be determined. To investigate the potential role of the caudate-putamen nucleus in experimentally induced tinnitus, we created a rat model of tinnitus induced by intraperitoneal administration of 350 mg/kg sodium salicylate. Our results revealed that the mean spontaneous firing rate of the caudate-putamen nucleus was increased by sodium salicylate treatment, while dopamine levels were decreased. In addition, electrical stimulation of the caudate-putamen nucleus markedly reduced the spontaneous firing rate of neurons in the primary auditory cortex. These findings suggest that the caudate-putamen nucleus plays a sensory gating role in sodium salicylate-induced tinnitus.