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Objective: To establish an animal model of brain injury in rats, the cognitive capacity to detect brain injury in rats, the determining factor detection point in time, and at the appropriate point in time detection of brain-derived neurotrophic factor (BDNF), N-methyl - D-aspartate receptor 1 (NMDAR1) content trends, preliminary study the relationship between cognitive impairment and brain injury and recovery. Method: 1. Establishment of animal models of brain injury in rats, normal SD male healthy rats 72 weight (230 ± 30) g by freefall combat establishment of brain damage model. According to the crackdown were divided into mild group, moderate injury group and hit the sham group. 2 time points to determine: the behavior of cognitive function by balancing test, walking test evade trial detection model change in the trend, and according to its changing characteristics determine the point in time of the detection. 3 at different time points on different parts of the brain brain tissue content of BDNF and NMDAR1 immunohistochemical detection and recording, analysis of BDNF and NMDAR1 in varying degrees of damage after content trends. Results: 1. Cognitive behavioral detection to determine the cognitive capacity to change the point in time after injury 1,2,4,7 days. Chemical detection BDNF immunohistochemistry: light, moderate brain injury group most serious the 2d cognitive impairment after injury, respectively 3,7 d after injury, returned to normal. Light, moderate brain injury group brain frontal cortex, hippocampus, basal forebrain region of brain-derived neurotrophic factor are increased after injury 1d was slowly increased and then reduced to a lower level in the 2d trend, with cognitive impairment The trend was synchronous changes and moderate brain injury group of brain-derived neurotrophic factor expression higher than the sham group with mild brain injury group (P lt; 0.05). Immunohistochemical detection NMDAR1: light, moderate brain injury in brain frontal cortex, hippocampus, basal forebrain area NMDAR1 after injury 1d higher to a lower level in the 2d and then was slowly increasing tendency with cognitive impairment trend was synchronous changes and moderate brain injury group NMDAR1 expression than the sham group with mild brain injury group (P lt; 0.05). Trend of two different factors with through behavioral cognitive testing cognitive impairment after injury trends, the two opposite effects, common cause changes in cognitive impairment in the acute phase after injury, BDNF play a more important role in the protection of neurons. Conclusion rat after traumatic brain injury, frontal cortex, the hippocampus and the BDNF and NMDAR1 content changes in the cells of the basal forebrain and injury cognitive impairment trend similarity; However, both counterproductive in cognitive impairments play a different role in the changes in the acute phase after injury, BDNF play a more important role in protecting neurons, BDNF expression in the hippocampus, basal forebrain is particularly evident changes, prompted in cognitive function in more a close relationship. Instead, NMDAR1 acute phase showed the damaging effects.
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