Effects Of GR Expression In Rat Hippocampus On Cognitive After Traumatic Brain Injury

Objective: Traumatic brain injury (TBI) is a complex pathological events such as neuronal degeneration, tissue loss to impaired neuronal plasticity , neurochemical dysregulation and so on. It has been proved that these events contribute to the observed cognitive and behavioral dysfunction. So we used the lateral head rotation device which was used in this study to explore the effect of GR expression in rat hippocampus on cognitive after traumatic brain injury and to look for the clinical treatment of brain protection of certain experimental basis.Methods: Healthy male Sprague-Dawley rats (200±20g) were purchased from the Center of Experimental Animal of Fourth Military Medical University. Rats were maintained in an environment with constant temperature, humidity, and free access to food and water, and a 12h light/dark cycle (07:00 to 19:00 per cycle). All measures were taken to minimize animal pain or discomfort. All experimental procedures were approved by the Chinese Small Animal Protection Association Production of animal model. All rats divided randomly into sham group (n=32) and TBI group (n=104). The latter was subdivided into 4 groups of 4 d, 5 d, 6d, 7 d. Some rats (sham no=8, TBI no=8) were used to test Morris water maze(MWW) and others (sham no=24, TBI no=96) for histological processing (n=40) and western blot (n=40) and RT-PCR (n=40). MWW test: Animals were always tested in the same order, using the same maze and spatial environment at approximately the same time each day. Rats received four trials per day over four consecutive days. For each trial, rats were placed into the water facing the wall, with the start locations varying randomly (N, NW, NE, SW, S, E or W), and permitted to swim until they reached the escape platform. A maximum of 120s was allowed before rats were placed on the platform. Once on the platform, rats remained there for 15s before being removed for an inter trial interval of 30min. Data on latency were plotted time to generate a spatial learning curve. To assess reference memory following a period of learning, a spatial probe test was given on the 7th day of MWM test. The hidden platform was removed from the pool and each animal was allowed to swim for 30s starting from the northwestern position. The experiments were started at 4d after TBI (to avoid animal motor dysfunction after TBI). Data are expressed as means±SD, unless otherwise indicated. Student's t test or ANOVA followed by Scheffés's test was used for statistical analysis as appropriate. Statistical significance was established at P < 0.05.Results: After traumatic brain injury, there is an extensive neuronal degeneration and necrosis in hppocampus CA1 Regulation, and this trend of the phenomena slowly go down as time went on. the GR expression in the hippocampus also showed a corresponding trend that GR expression in hippocampus after injury showed a downward trend. At 6d after traumatic brain injury, the GR expression is the most significant. Morris water maze test: The control group and TBI group were trained in the spatial learning task at same time. To assess GR protein changes in hippocampus, the spatial memory of rats was tested in MWM, which tests rats'ability for spatial learning and memory by measuring a rat's ability to navigate and exploration. According to the data of experiment, latency was shortened during the 4-day acquisition period. But latency of TBI group was more long than sham. AT 7d after TBI, The number of TBI group cross-platform was more than sham.Conclusion: According to the lateral head rotation device, we have set up TBI rat model, and examined changes in dysfunctions in rats subjected to experimentally controlled TBI and correlated such changes to glucocorticoid receptor in hippocampus. We observed that rats developed learning and memory deficiency after TBI, and the lower hippocampal GR express, the worse the deficiency was.