A large body of evidence shows that spinal circuits are significantly affected by training, and that intrinsic circuits that drive locomotor tasks are located in lumbosacral spinal segments in rats with complete spina...A large body of evidence shows that spinal circuits are significantly affected by training, and that intrinsic circuits that drive locomotor tasks are located in lumbosacral spinal segments in rats with complete spinal cord transection. However, after incomplete lesions, the effect of treadmil training has been debated, which is likely because of the difficulty of separating spontaneous stepping from specific training-induced effects. In this study, rats with moderate spinal cord contusion were sub-jected to either step training on a treadmil or used in the model （control） group. The treadmil training began at day 7 post-injury and lasted 20 ± 10 minutes per day, 5 days per week for 10 weeks. The speed of the treadmil was set to 3 m/min and was increased on a daily basis according to the tolerance of each rat. After 3 weeks of step training, the step training group exhibited a sig-nificantly greater improvement in the Basso, Beattie and Bresnahan score than the model group. The expression of growth-associated protein-43 in the spinal cord lesion site and the number of tyrosine hydroxylase-positive ventral neurons in the second lumbar spinal segment were greater in the step training group than in the model group at 11 weeks post-injury, while the levels of brain-derived neurotrophic factor protein in the spinal cord lesion site showed no difference between the two groups. These results suggest that treadmil training significantly improves functional re-covery and neural plasticity after incomplete spinal cord injury.展开更多
Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]....Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor （BDNF） [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] （Fig. 1C）. To determine the rela- tionship between the gliogenic LTP and high frequency stimulation （HFS）-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP （Fig. 1A）. Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP （Fig. 1B）.展开更多
Following central nervous system injury, axonal sprouts form distal to the injury site and extend into the denervated area, reconstructing neural circuits through neural plasticity. How to facilitate this plasticity h...Following central nervous system injury, axonal sprouts form distal to the injury site and extend into the denervated area, reconstructing neural circuits through neural plasticity. How to facilitate this plasticity has become the key to the success of central nervous system repair. It remains controversial whether fine motor skill training contributes to the recovery of neurological function after spinal cord injury. Therefore, we established a rat model of unilateral corticospinal tract injury using a pyramidal tract cutting method. Horizontal ladder crawling and food ball grasping training procedures were conducted 2 weeks before injury and 3 days after injury. The neurological function of rat forelimbs was assessed at 1, 2, 3, 4, and 6 weeks after injury. Axon growth was observed with biotinylated dextran amine anterograde tracing in the healthy corticospinal tract of the denervated area at different time periods. Our results demonstrate that compared with untrained rats, functional recovery was better in the forelimbs and forepaws of trained rats. The number of axons and the expression of growth associated protein 43 were increased at the injury site 3 weeks after corticospinal tract injury. These findings confirm that fine motor skill training promotes central nervous system plasticity in spinal cord injury rats.展开更多
基金sponsored by the National Natural Science Foundation of China,No.30872604,81171862
文摘A large body of evidence shows that spinal circuits are significantly affected by training, and that intrinsic circuits that drive locomotor tasks are located in lumbosacral spinal segments in rats with complete spinal cord transection. However, after incomplete lesions, the effect of treadmil training has been debated, which is likely because of the difficulty of separating spontaneous stepping from specific training-induced effects. In this study, rats with moderate spinal cord contusion were sub-jected to either step training on a treadmil or used in the model （control） group. The treadmil training began at day 7 post-injury and lasted 20 ± 10 minutes per day, 5 days per week for 10 weeks. The speed of the treadmil was set to 3 m/min and was increased on a daily basis according to the tolerance of each rat. After 3 weeks of step training, the step training group exhibited a sig-nificantly greater improvement in the Basso, Beattie and Bresnahan score than the model group. The expression of growth-associated protein-43 in the spinal cord lesion site and the number of tyrosine hydroxylase-positive ventral neurons in the second lumbar spinal segment were greater in the step training group than in the model group at 11 weeks post-injury, while the levels of brain-derived neurotrophic factor protein in the spinal cord lesion site showed no difference between the two groups. These results suggest that treadmil training significantly improves functional re-covery and neural plasticity after incomplete spinal cord injury.
文摘Long-term potentiation （LTP） at synapses between primary afferents and spinal dorsal horn neurons induced by noxious electrical stimulation or injury of peripheral nerve is con- sidered to underlie chronic pain [1]. The mechanisms of the spinal LTP have been intensively investigated, since it was discovered in 1995 [2]. In recent years, spinal application of ATP [3], brain-derived neurotrophic factor （BDNF） [4] and opioid [5] has been shown to induce spinal LTP at C-fiber synapses in the absence of conditioning activation of primary afferents. This is contrary to the general belief that coinci- dent pre- and postsynaptic activity is needed for LTP induction. Recently, Sandkiihler and his co-workers reported in Science that combined activation of microglia and astro- cytes by P2X7 receptor agonist BzATP induces LTP at synapses between afferent C-fibers and spinal lamina I neurons in the absence of presynaptic activation, which is termed gliogenic LTP [6] （Fig. 1C）. To determine the rela- tionship between the gliogenic LTP and high frequency stimulation （HFS）-indueed LTP, they used transverse lum- bar spinal cord slices with long dorsal roots which were separated into halves. Twenty two lamina I neurons that received independent monosynaptic C-fiber inputs from each dorsal root half were recorded. Homosynaptic LTP is recorded in 12 neurons, among them 6 neurons also show heterosynaptic LTP （Fig. 1A）. Interestingly, heterosynaptic LTP is also induced in 5 neurons in which HFS fails to induce homosynaptic LTP （Fig. 1B）.
基金supported by the National Natural Science Foundation of China,No.30972153
文摘Following central nervous system injury, axonal sprouts form distal to the injury site and extend into the denervated area, reconstructing neural circuits through neural plasticity. How to facilitate this plasticity has become the key to the success of central nervous system repair. It remains controversial whether fine motor skill training contributes to the recovery of neurological function after spinal cord injury. Therefore, we established a rat model of unilateral corticospinal tract injury using a pyramidal tract cutting method. Horizontal ladder crawling and food ball grasping training procedures were conducted 2 weeks before injury and 3 days after injury. The neurological function of rat forelimbs was assessed at 1, 2, 3, 4, and 6 weeks after injury. Axon growth was observed with biotinylated dextran amine anterograde tracing in the healthy corticospinal tract of the denervated area at different time periods. Our results demonstrate that compared with untrained rats, functional recovery was better in the forelimbs and forepaws of trained rats. The number of axons and the expression of growth associated protein 43 were increased at the injury site 3 weeks after corticospinal tract injury. These findings confirm that fine motor skill training promotes central nervous system plasticity in spinal cord injury rats.
