| The treatment of spinal cord injury (SCI) remains to be a puzzling and challenging issue in medical science. To date, the main directions in the research work of SCI are: (i) to rescue the injured neurons from secondary injury and death; (ii) to promote axonal regeneration by application of neurotrophins (NTs) and/or blocking the neurite growth inhibitors; (iii) neural transplantation including fetal CNS tissue, neural stem cells, and Schwann cells, et al; (iv) to gain remyelination of the injured axon and recover the axon conduction; and (v) to enhance the plasticity, including the collateral sprouting of undamaged axons and the efficiency of synaptic transmission, after incomplete SCI (iSCI).The plasticity of central nervous system (CNS) can be defined as the potential or ability for change, which can be explored both during development and maturity by the imposition of transient or stable abnormal circumstances or injury that disrupt the normal condition. There is often a remarkable degree of spontaneous function recovery after iSCI both clinically and in animal experiments, even in the absence of treatment. Plasticity is considered to be the main mechanism of the spontaneous function recovery in a more protracted period, ie several weeks to years after injury. After iSCI, the plasticity can occur at cortex, subcortical level, the spinal cord itself and peripheral organs, which include three forms: (i). enhancement of the efficiency of synaptic transmission in existing circuitry; (ii). formation of new circuitry by collateral sprouting and structural rearrangement; and (iii). activation of the circuitry which are functional-latent in normal condition and undamaged by the injury, such as the crossed phrenic phenomenon(CPP). Sprouting is one of the most important forms of plasticity in CNS, which is considered to play an important role in learning, skill acquisition, repair in CNS injury and diseases, and formation of some pathological conditions.After SCI, certain degree of plasticity can occur in adult animals but with declining potential when the animals become mature. The existence of neurite growth inhibitors and the lack of NTs are thought to be the main reason for this phenomenon. And now, application of NTs to CNS by adenovirus-mediated gene transfer has become one most useful strategy totreat CNS trauma and diseases.Spontaneous recovery of locomotion can occur after transection of T11 or T 12 spinal cord in rats and cats and treadmill training can enhance this recovery. Central pattern generator (CPG) that locates at the upper lumbar spinal cord is thought to be the substrate of this recovery. And inhibitory transmitter system involves in this procedure, too. So we want to ask, after cervical SCI, whether fine movement of forelimb recovery can be obtained by training. In the present study, we amplified, purified and identified the AxCA-BDNF and AdCMV-huCT1 recombinant adenovirus vector (RAD) at first. Then we explored the effects and the possible mechanisms of adenovirus-mediated BDNF and huCT-1 gene transfer and training on plasticity after incomplete SCI in rats.Main Methods and Techniques:1. 293 cells were employed as the package cell to amplify the RAD. Purification of RAD was obtained by CsCL density gradient centrifugation. RAD was identified by PCR, RT-PCR and immunocytochemistry at DNA, RNA, and protein level, respectively. The titer of RAD was examined by plaque forming test.2. Stereotaxically, cervical dCST and red nuclei were injured by transection and injection of quinolic acid (QA), respectively. Toluidine blue staining and HE staining were employed to assess the extent of the injuries. Biotin Dextran Amine (BDA) was injected to the somatosensory cortex to visualize the sprouting of ventral CST. The rats' forelimb performance test was modified and used to examine the rats' forelimb function.3. Eighty-eight rats were divided into 5 groups randomly: normal group (N group), injury group (I group), BDNF group, CT-1 group and training group (T group). After combine...
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