Objective To discuss about the establishment of mental depression model by traumatic brain injury in rats,and to evaluate the validity of this model.Methods The study was carried out in the experiment center of Wuhan University.A total of 48 male adult Wistar rats were randomized ( random number) into four groups ( n =12,each):( 1 ) in sham operation group,six rats were fed normally in one cage; (2) in model group,the model of the left frontal lobe contusion was made up by hitting with free-fall method on the left cortex of the rat,and subsequently the each of model rats were separately fed in a cage and put them in a lonely environment with chronic stress one week after traumatic brain injury in order to induce them into models of mental depression; ( 3 ) in brain trauma group,the trauma model of the left frontal lobe contusion was set up by the same procedure as in model group,and six rats were fed together in one cage; (4) in CUMS group,each rat was fed normally in one cage in a lonely environment after brain trauma made and chronic mild chaotic stress unpredictable to rats was given to induce mental depression.The consumption of sucrose water and the change of animal behavior were observed and the high performance liquid phase electrochemical with fluorescence detector was used to detect the biogenic monoamine neurotransmitter content (dopamine,serotonin and norepinephrine) in the hippocampus,prefrontal cortex,hypothalamus and striatum area in each group.Experimental data were processed with single factor analysis or t test of variance by Statistical Program for Social Sciences Version 13.0 (SPSS13.0) software.P ＜0.05 was considered as statistically significant difference.Results After modeling,the rats of four groups were examined by behavioral tests.It was found that the amount of sugar-water consumption by the rats in the model group and CUMP group decreased,implying the absence of interest in eating and anhedonia of the rats in these groups.In open-field test,the rats in the model group,CUMP group and brain trauma group showed reduction in square crossing and rearing,implying the under-activity and absence of interest in activity.In the water maze test,it was found that the rats in the model group,CUMP group and brain trauma group needed much time to reach the end-point and made many errors,implying the lowering ability to learn and memorize.Levels of dopamine,serotonin and norepinephrine in the hippocampus,prefrontal cortex,hypothalamus and striatum area decreased in these rats with traumatized brain in three groups especially in model group and CUMP group.Conclusions It is a valid method for establishing the mental depression model in rats by traumatic brain injury with separately feeding in the lonely environment and given chronic mild chaotic stress unpredictable to rats on the setting of the left frontal lobe contusion.

Objective To determine the intervention of mycophenolate mofetil (MMF) in glial scar formation and learning and memory function in a rat model of diffuse axonal injury (DAI).Methods Ninety-six SD rats were randomly divided into sham group, normal saline (NS) group and mycophenolate mofetil (MMF) group according to the random number table, with 32 rats per group.Immunohistochemistry was used to detect activated microglia cells, activated astrocytes and chondroitin sulphate proteoglycanns (CSPGs) in the hippocampus.Inage-Pro Plus software was used to quantitatively assess the changes of activated microglia cells, activated astrocytes and CSPGs.Morris water maze was applied for testing rat learning and memory function.Integrated absorbance (IA) of major constituents (microglia, astrosyte, chondroitin sulphate proteoglycan) of the glial scar was determined and analyzed for the correlation with the parameters of MWM.Results At 7, 14 and 28 days after injury, MMF group showed decreased IA of activated microglia in the hippocampus compared to sham and NS groups (P ＜ 0.05).At 7-11 days after injury, percent distance and percent time in the target quadrant of Morris water maze did not differ significantly among the three groups and were not related to the IA of glial scar.At 28-32 days after injury, percent distance and percent time in the target quadrant of Morris water maze lowered significantly in MMF group.At 28 days after injury, IA of the glial scar had a positive correlation with mean speed and mean escape latency, but negative correlation with percent distance and time in the target quadrant that measured in Morris water maze at 28-32 days after injury.Conclusion MMF significantly attenuates glial scar formation into the hippocampus and improves learning and memory function in rats during the recovery stage when administered in the early stage after DAI.

Objective To investigate the effects of human Rrain-derived neurotrophic factor-gamma fetopro-tein (hBDNF-GFP) gene-transfected neural stem cell (NSC) transplantation on BDNF expressions in the retina of rots after optic nerve (ON) crush injury. Method ①Seventy-eight Sprague-Dawley (SD) rats were randomly as-signed into a control group (n = 6) and ON crush group (n = 72). In the ON crush group, the right ON was crushed while the left NO was exposed as sham injury. Rats in the ON crush group were divided into three sub-groups: PBS group (intravitreons injection of 0.01 mol/L phosphate buffered solution); GFP group (intravitreous transplantation of GFP gene-transfected NSCs); and hBDNF-GFP group (intravitreous transplantation of hBDNF-GFP gene-transfected NSCs). Rats were sacrificed 3, 7, 14 and 28 days after transplantation, and BDNF expres-sions in retinal homogenates was detected by using enzyme-linked immunosorbent assay (ELISA). ②The hBDNF-GFP-NSCs were transplanted intravitreous into six rats after ON crush injury. Following this, two rats were sacri-riced 2, 4 and 8 weeks after transplantation. The survival and location of NSCs in host retina were observed by frozen section analysis. ③Adult SD rats were randomly divided into four groups: control group (n = 5); NSC group (NSC transplantation, n = 10); GFP-NSC group (GFP-NSC transplantation, n = 10); and hBDNF-GFP-NSC group (hBDNF-GFP-NSC transplantation, n = 10). Four and eight weeks after transplantation, five rats from every group were sacrificed. Western blot analysis was used to determine retinal BDNF expression. Results ① There was no significant difference in BDNF expression between the control group and sham-injury groups (P >0.05). Three days after NSC transplantation, BDNF expression increased significantly in the three injured sub-groups compared with the sham-injury group, (P < 0.05), whereas no significant inter-group differences in BDNF expressions among three injured sub-groups were observed (P > 0.05). Seven days after transplantation, there was a significant difference in BDNF expression between the GFP-NSC group and the sham-injury groups (P <0.05), whereas there were no significant differences in BDNF expressions among the PBS, hBDNF-GFP-NSC and sham-injury groups (P > 0.05). Fourteen and 28 days after transplantation, BDNF expressions decreased in the PBS group and the GFP-NSC groups, while BDNF expressions in the hBDNF-GFP-NSC group increased significant-ly compared with the other three groups (P < 0.05); ②Frozen section showed that transplanted hBDNF-GFP-NSCs could survive and gradually extended to all layers of the host retina. ③Westem blot revealed there were no differences in BDNF expressions between 4-week and 8-week intervals in the hBDNF-GFP-NSC group. Compared with other three groups, BDNF expressions in the retina increased significantly after hBDNF-GFP-NSC transplanta-tion. Conclusions The hBDNF-GFP gene-trausfected NSCs can survive in the host retina and BDNF expressions are stable at a high level.

ObjectlveTo evaluate the role of cannabinoid receptor 2 (CB2 receptor) in microglial injury induced by glutamate.MethodsMicroglia cells were randomly divided into 4 grups:control group (group C),microglial injury group ( group Ⅰ),specific CB2 receptor agonist AM 1241 group ( group AM1241 ) and specific CB2 receptor antagonist AM630 group (group AM630).In group C,the cells were cultured routinely for 26 h.In group Ⅰ,the cells were incubated in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM1241,the cells were incubated in the culture medium containing AM1241 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.In group AM630,the cells were incubated in the culture medium containing AM630 2 μmol/L for 2 h,and then in the culture medium containing glutamate 10 mmol/L for 24 h.The cell viability and release of LDH were measured.Microglial morphology was observed under microscope.Results Compared with group C,the cell viability was significantly decreased,and the release of LDH was significantly increased in groups Ⅰ,AM1241 and AM630 (P ＜ 0.05).Compared with group Ⅰ,the cell viability was significantly increased,and the release of LDH was significantly decreased in group AM1241 ( P ＜ 0.05).There was no significant difference in the cell viability and the release of LDH between groups 1 and AM630 ( P ＞ 0.05).Conclusion Glutamate induces microglial injury through inhibiting the function of CB2 receptor.

Objective To observe the spatiotemporal characteristics of the micro-structural injury in a rat model of diffuse axonal injury (DAI) and quantitatively assess the axonal injury severity in the vulnerable areas. Methods The 7.0 T MRI was performed in rats in DAI group (n =20) and control group ( n = 15 ) to synthesize the diffusion tensor imaging ( DTI) parameter map and calculate the parameter value of the vulnerable areas. Immunohistochemistry was used to detect β-APP expression in the vulnerable areas and the IPP software to quantitatively assess the axonal injury severity. Results Compared with the control group, FA and AD maps showed local signal defection or reduction in the corpus callosum and their values decreased significantly in the brain stem and corpus callosum in the DAI group (P ＜0.01 ). The integrated optical density (IOD) value of the vulnerable areas in the DAI group was significantly higher than that of the control group ( P ＜ 0. 01 ) , with the highest level in the brain stem (P＜0.05). The normalized FA, AD and ADC in the vulnerable areas were correlated negatively with the IOD (P ＜ 0.05). Conclusion DTI can detect invisible micro-structural injury in the vulnerable areas and quantitatively assess the axonal injury severity in vivo in the early stage.

Objective To investigate the changes of expression of stromal cell-derived factor 1α (SDF-1α) in retinas after partial optic nerve injury in rats. Methods Models with injury of partial optic nerve were induced in rats. Retinal tissues were collected 1,2,3,5,7,10 and 14 d after injury. Enzyme linked immunosorbent assay and Real-time quantitative PCR were employed to detect the expression of SDF-1α protein and mRNA in retinal tissues respectively in injury group (n=28), sham operated group (n=28) and normal control group (n=12). Results The expression of SDF-1α protein and mRNA in retinas was higher than that in sham operated group and normal control group at different time points after injury (P<0.01), and it reached the peak at the 5th day after injury. The expression of SDF-1α protein and mRNA maintained a high level at the 14th day after injury. Conclusion The expression of SDF-1α protein and mRNA is up-regulated after partial optic nerve injury, and may last for a long time.

Objective To analyze the effects of mild traumatic brain injury ( mTBI) on functional brain network parameters and to study the properties of small world of patients. Methods Ten patients with mild traumatic brain injury and 13 healthy controls matched by age and sex were collected from the Ninth People's Hospital Affiliated to Medical College of Shanghai Jiao Tong University. Resting functional magnetic resonance images of all subjects were collected. Functional networks were constructed and brain network properties were analyzed. Results The brain injury group and the healthy control group had small world at-tributes in the selected sparseness range. The global efficiency of patients with mTBI patients was significantly reduced compared to healthy control group (0. 174±0. 141 vs 0. 184±0. 062),t=2. 417,P=0. 025),and the shortest path length was increased compared to healthy control group (0. 797±0. 930 vs 0. 734±0. 488),t=-2. 083,P=0. 048). Conclusion The functional brain network of patients with mTBI patients has small world attributes,and the parameters of functional brain network of patients have changed.

Objective, accurate and noninvasive assessment of the condition and prognosis of traumatic brain injury (TBI) patients in the early stage is the basis of TBI treatment. Glasgow coma scale (GCS) is the most common clinical method for assessing trauma condition. However, when patients are sedated, intubated or have language or movement disorders, it is often impossible to make an accurate assessment by GCS. In addition, GCS cannot provide direct evidences of pathological damage in brain tissues. The CT scoring system has emerged in recent years and is a non-invasive evaluation system based on CT images. The evaluation process can objectively reflect the severity of brain tissue damage without being interfered by sedation or intubation. The authors review the progress of researches on CT scoring systems to assess the prognosis of patients with craniocerebral injury, so as to provide a reference for clinicians to choose appropriate injury assessment methods and make clinical decisions.