Project description:This study aimed to explore the possible mechanism of lidocaine-induced neurotoxicity. A total of 40 rats were randomly assigned to 4 groups (n = 10 per group): control group; sham group, received only intrathecal catheter insertion; saline group, received an intrathecal injection of saline; and lidocaine group, received an intrathecal injection of 10% lidocaine. Neurobehavioral tests were performed on rats in each group before injection and 1, 2, 3, and 4 days after the intrathecal injection. On the fourth day, after completing neurobehavioral tests, the spinal cords of all rats from L2 to L6 were removed and immediately stored in liquid nitrogen. In the control and lidocaine groups, parts of the spinal cord tissues of three rats were selected for gene microarray analysis.Based on the results of the gene chip analysis,Five rats in each group underwent real-time quantitative polymerase chain reaction (PCR) and five Western blot analysis to verify Differentially expressed genes at the mRNA transcription and protein levels. The aim of gene chip analysis is to screen potential genes involved in lidocaine-induced neurotoxicity.
Project description:The aneurysm clip impact-compression model of spinal cord injury (SCI) in animals mimics the primary mechanism of SCI in human, i.e. acute impact and persisting compression; and its histo-pathological and behavioural outcomes are extensively similar to the human SCI. In order to understand the distinct molecular events underlying this injury model, an analysis of global gene expression of the acute, subacute and chronic stages of a moderate to severe injury to the rat spinal cord was conducted using a microarray gene chip approach. Rat thoracic spinal cord (T7) was injured using aneurysm clip impact-compression injury model and the epicenter area of injured spinal cord was isolated for RNA extraction and processing and hybridization on Affymetrix GeneChip arrays.
Project description:Biomarkers to more accurately determine severity and prognosis following spinal cord injury (SCI) are needed to ensure that patients are assigned to the most suitable treatment and rehabilitation regimes. This study aimed to characterise the blood proteome following SCI in clinical rat injury models to identify novel candidate biomarkers and altered biological pathways.
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomenon we examined the transcriptional response of the motor neurons after spinal cord injury. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurons 21 and 60 days after complete spinal transection where the tail exhibits clear signs of spasticity.
Project description:To investigate the mechanism of electrical stimulation in the repair of spinal cord injury, we established a rat model of spinal cord injury. Then, we used RNA-SEQ data obtained from ES treatment and 6 different rat models of spinal cord injury for gene expression profile analysis.
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalization. To understand the molecular mechanism behind this phenomenon we examined the transcriptional response of the motor neurons after spinal cord injury. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurons 21 and 60 days after complete spinal transection where the tail exhibits clear signs of spasticity. Tail MNs were retorgradely labelled with flourogold injected into the muscle and intra peritoneally. 5-7 days after tracer injections the spinal cord was dissected out, snab frozen in liquid nitrogen, sliced in 10 um thick slices and fluorescent motor neurons were laser dissected into a collector tube to a total of ca. 50-200 cells pr sample. RNA was then extracted, two round amplified and hybridized to Affymetrix rat 230 2.0 arays. 27 samples were hybridized onto chips, 8 Spi-21, 8 Spi-60, 6 ShamC-21 and 5 ShamC-60.
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalizaion. To understand the moleclar mechanism behind this pheneomona we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after comlete spinal transection.