Objective To research the effects of tianeptine and lithium on expression of pCREB in hippocampus of chronic stress depression rats. Methods All the experimental rats were divided by random into : Group of depression,Group of tianeptine,Group of lithium and Group of control. The rats of Group of depression, Group of tianeptine and Group of lithium were applied stress for 21 days,and meanwhile Group of control had no stress. The rats of Group of tianeptine were fed with tianeptine (50 mg/kg) , Group of lithium were fed with lithium (60 mg/kg) , while another groups were fed with normal sodium of the same volume. The ethology examination was performed by using method of open-field and experiment of fluid consumption. The expression of pCREB was detected by Western-blotting method. Results After the chronic stress,the horizontal crossing numbers,the erection times,the modification times and the percentage of sacchar-consumption of the rats of Group of depression were 23.2±23.0;8. 1 ±7.2; 3.6 ±3.5 and (55.4 ±11.7)% respectively, which were less than Group of control (46.0±18.9;20.3±11.3;8.4±2.7 and (68.5 ±8.2)% ; P＜0.01). The horizontal crossing numbers(28. 1 ±23.0) ,the erection times(12. 1 ± 9.4) and the modification times(5.5 ±3.2) of Group of tianeptine are less than those of Group of control (P ＜ 0. 05), but no significant difference compared with Group of depression; the percentage of sacchar-consumption(62.7 ± 10.6) % ,Group of tianeptine was more than Group of depression (P＜ 0.05 ) , but no obvious difference with Group of control. The horizontal crossing numbers, the erection times, the modification times and the percentage of sacchar-consumption of Group of lithium were less than those of Group of control (P ＜ 0.05), more than those of Group of depression but no significant difference (P ＞ 0.05). In Westernblotting method,the level of pCREB in the hippocampus of Group of depression was less than that of Group of control (P＜ 0.01); that of Group of tianeptine was more than that of Group of depression (P ＜ 0.01) but no obvious difference with Group of control; that of Group of lithium was less than that of Group of control (P＜0. 01) and more than Group of depression (P＜0.01). Conclusion Tianeptine could reverse the reduction of expression of pCREB in hippocampus of chronic stress depression rats and lithium partly did it.

Objective To investigate the effects of different concentrations of isoflurane on the caspase-3 expression in the hippocampus and S100β level of plasma in fetal rats. Methods 18 pregnant rats at gestational day 21 were divided into control group, 1. 3% isoflurane group,3% isoflurane group. Rats in the control group spontaneously breathed 100% oxygen for 1 h. Rats in the treatment groups breathed 1.3% or 3% isoflurane in 100% oxygen through an endotracheal tube, with mechanical ventilation for 1 h. Rat pups were delivered by cesarean section 6 h after treatment, and fetal blood was sampled from the left ventricle of each fetal heart and evaluated for S100β. Fetal brains were then evaluated for apoptosis, using caspase-3 immunohistochemistry in the CA1 region of the hippocampus. Results Compared to the control group ((1. 48 ± 0. 08) μg/L) and the 1. 3% isoflurane group( (1.53 ±0. 12)μg/L) ,the 3% isoflurane group showed significantly higher level of S100β( (3. 12 ±0. 15) μg/L, P＜0.05) . There was no differences in densities of caspase-3-positive cells between the control ((33 ±4) cell/mm ) and 1.3% isoflurane groups((31 ±5)cell/mm2). Compared to 1.3% isoflurane,isoflurane at a concentration of 3%((75 ± 7) cell/mm2, P＜0.05) for lh increased neurodegeneration in the hippocampal CA1 area in the developing brain of fetal rats. Conclusion Isoflurane can dose-dependently induce brain damage. Isoflurane at a concentration of 3% for lh can induce apoptosis in the hippocampal CA1 area and increase S100β levels of fetal rats.

Objective To investigate whether there is correlation exists in the effection of chronic unpredictable stress on active avoidance behavior and electroencephalogram ( EEG) of rat. Methods Twenty male SD rats (weight～200 g) were randomly divided into control group( n= 10) and model group( n- 10). Rats in model group were subjected to chronic unpredictable stress . Active avoidance response were observed with GeminiTM avoid system and EEG power spectrum was evaluated with Powerlab system. Results The failure rate in active avoidance test was correlation with delta wave power in EEG. Compared with control group, rats in model group had reduced failure rate in active avoidance task(42 ±36)% vs (82 ±30)% , P＜0.05). The EEG power spectrum of model group rats increased in delta band((47.09 ±22.86)μV2 vs (22. 55 ± 11. 57) μV2, P＜0. 05), which had the significant difference between the two group rats. The failure rate of active avoidance task in model group rats was positive correlation with EEG power spectrum of delta wave (r = 0. 717, P ＜ 0. 05) . Conclusion Chronic unpredictable stress facilitated active avoid behavior and changed spontaneous EEG, which suggested chronic unpredictable stress actived the neurotransmitter network system involved with active avoidance task in central nervous system. Brain cognitive function correlated positively with brain electrophysiology activity measured in chronic unpredictable stress induced rat model.

Objective To investigate the changes and mechanism of learning and memory in rats by different doses of benzo (a) pyrene (B(a)P). Methods Forty weaned rats (28 days) were randomly divided into control group (NS), solvent group ( vegetable oil) and three B (a) P dosage groups (the doses were 5,10 and 20 mg / kg body weight respectively ). And all rats were administrated intraperitoneally every other day to one month. The capability of learning and memory in rats were measured by Morris water maze test, and the brain-derived neurotrophic factor ( BDNF) and NMDAR2B content in hippocampus were tested by immunohistochemistry. Results In training of Morris water maze,the average escape latency was extended gradually with increasing dose, and there was a statistically significant difference between high-dose group((62. 78 ±47. 25 )s) and the control group((40.60±38.79)s)(P＜ 0.01). Compared with the control group(11.25 ±2.63), the number of crossplatform of high-dose group(4.33 ±2.08) was statistically reduced (P＜0.05). B(a)P at 10 and 20 mg/kg decreased NMDAR2B and BDNF expression in hippocampus of rats in immunohistochemistry. The level of NMDAR2B was (162.23 ±6.56) in the high-dose group and (150.38 ± 15.34) in the control group(P＜0.05);the expression level of BDNF was (163. 13 ± 8.09) in the high-dose group and (141.83 ± 13.37) in the control group(P＜ 0.05). Conclusion Subacute B(a)P exposure can reduce spatial learning and memory in weaning rats, it may be related to decreased levels of NMDAR2B and BDNF in hippocampus.

Objective To investigate the influence on the behavior of withdrawal and relapse after deep brain stimulation of bilateral nucleus accumbens in morphine-dependent rats. Methods The rats with a strong unconditioned preference were discarded in preconditioning test, the selected rats were distributed into five groups randomly. After operation,morphine hydrochloride was injected subcutaneously into SD rats for 12 days (once every day,initial 5 mg/kg,increasing by 5 mg/kg per time,stable in 20 mg/kg ). A modified electrical circuit was used to procedure the DBS,the parameter was 130 Hz,150 A,60 s,l h/d,14 d. CPP test was used to exam the effect of DBS. A minor morphine dose (3 mg/kg) was injected to induce the behavior of relapse, and CPP was tested again after 24 h. Two-way ANOVA was performed on the data with Bonferroni posttest. Result ①After CPP training,CPP score of group morphine, morphine + sham and morphine + DBS was ( 155. 87 ± 20. 45 ) s, (107.33 ± 18.10)s,(135.45 ±22.09)s,and had significant difference with group of control( ( -70.34 ± 15.40) s)(t = 9.45,P＜0.01; t = 6.94,P＜0.01;t = 8.04,P＜0.01).②After 7 days' DBS,the CPP score in group of morphine + DBS reduced significantly compared to group of morphine( t = 4.21, P＜0.01) and morphine + sham( t=1.10, P＜0.05).0n the 14th day,there was more pronounced reduction ( t = 5. 15, P＜0.01; t = 3.92, P＜ 0.01). ③ 24 hours after the minor morphine dose was injected,the CPP score in morphine + DBS didn't increase significantly, and had significant difference with group of morphine ( t = 4.04, P＜0.01) and morphine + sham ( t= 4. 13, P＜0.01). Conclusion DBS bilateral nucleus accumbens in morphine-dependent rats can interfere the behavior of morphine-induced CPP and relapse.

Objective To observe the effects of the extract from daylily on the learning and memory in depression model rats, and to explore its possible mechanism. Methods Rats were randomly divided into control group, model group ( CUMS), the positive group (CUMS + fluoxetine) , high, medium and low dose group (stress + daylily extract in different doses), 12 rats in each group. The depression model was established by combining separation and chronic unpredictable stress. Body mass, open-field-test and sugar consumption experiment were used to evaluate the changes of behaviors in rats. And morris water Maze test was used to evaluate the ability of learning and memory. Results There was no statistically distinction between the rats of each group on weight and the behavioral indicator before modeling. Compared with the control group, the vertical movement,horizontal movement of open box test in the model group were reduced (P＜0.05 ) ,and sugar consumption and preference degree decreased (P<0.05 ).The target quadrant time, platform resident time, effective area residence time and crossing platform times in the water maze test of the model group was less than those of the control group. The daylily effect was evaluated at 0, 7, 14, 21, 28, 35, 42 days respectively post treatment. There were significant differences in depression behaviors between model group and daylily group(P＜0.05). And each indicator in the water maze test of the daylily group (high, medium dose) was more than that of model group (P ＜ 0. 05). Control group, model group, positive group, high, medium and low dose group, vertical movement scores were (41.83 ± 17.63; 8.14 ±4.23; 12.73 ±7.21; 23.17 ± 18.75; 8.38 ±3.46; 13.50 ±5.44); horizontal movement scores were (69.92 ±34.04; 28.33 ±20.36; 62.25 ± 15.72; 69.42 ±35.17 ; 49.08 ±32.85; 48.08 ±21.19). Conclusion Daylily may be partially work on the depression of rats, with some antidepressant effect, meantime,daylily can improve the ability of learning and memorizing of the depressed rats.

Objective To determine the effects of genistein and daidzein on the proliferation and survival of the hippocampal neural cells and underlying mechanism. Methods H19-7/IGF-IR neural cell line was cultured in phenol red free DMEM absented of serum for 72h. Genistein, daidzein or 17β-estradiol was added to the culture at various concentrations. Their proliferation and protective effects on the neuronal cells were determined by BrdU and MTT assay respectively. The effect of phytoestrogens on cell cycle regulation was determined using flow cytometry. The effects of the soy isoflavones on brain-derived neurotrophic factor (BDNF) expression were determined by ELISA and RT-PCR respectively. Results It was observed that, with 72h of treatment, 20nM and 200 nM 17B-estradiol significantly promoted the neuronal cell proliferation at 33% and 36% ;20nM and 200nM genistein significantly promoted the neuronal cell proliferation at 15% and 13% ; 200nM daidzein significantly promoted the neuronal cell proliferation at 11% compared to the control (P＜0.05). Genistein and daidzein induced an significantly increase in the S phase arrest at (17.64 ± 0.43) % and (19.48 ± 1.01) % compared to the control (P ＜ 0. 05). Moreover, genistein and daidzein significantly increased the expression of mature BDNF and BDNF mRNA level (P＜0.05). The effect of genistein and daidzein on hippocampal neuronal cell proliferation was blocked by K252a, selective inhibitor of tyrosine kinase receptors. Conclusion Genistein and daidzein improved hippocampal neuronal cell proliferation and viability in vitro. The effects might be mediated by increasing in BDNF expression.

Objective To investigate correlation between the amount of interleukin-17 (IL-17) producing cells and the expression of transforming growth factor (31 (TGF-β1) in glioma,and evaluate the clinical values of IL-17 and TGF-pl in predicting the prognosis of glioma. Methods The presence of IL-17 and TGF-pl was measured by immunohistochemistry in 135 human glioma (WHO Ⅰ 18,WHO Ⅱ 45,WHO Ⅲ 53,WHO Ⅳ 19) tissues and 15 normal brain tissues. Results There was no IL-17 positive staining in normal brain tissues. Of 135 glioma specimens showed low TGF-pl expression and 77 (57. 03% ) showed high TGF-pl expression. No TGF-β1 expression was detected in normal brain tissue. Furthermore,TGF-β1 expression was positively correlated with the amount of IL-17 producing cells in glioma tissues ( r=0.285, P<0.01). Compared with the low grade,the levels of IL-17 and TGF-pl positive cells were obviously increased in high grade. The Kaplan-Meier analysis showed that there were significant differences in overall survival (OS) between the IL-17 and TGF-pl high-expression and lowexpression group (P＜0.01, P＜0.05). The 3-year OS rates of IL-17 of high expression and low expression were 33.75% and 76. 36%. Multivariate Cox proportional hazards regression analysis indicated that age,KPS score, IL-17 were independent prognostic factor for OS (P＜0.01). Conclusion Intratumoral IL-17-producing cell density and the expression of TGF-β1 was associated with the malignancy of human glioma.

Objective To investigate the alteration of nuclear factor kappa B( NF-κB) and tumor necrosis factor-a (TNF-α) mRNA and protein in hippocampus in chronic constrictive injury (CCI) model of rats. Methods Seventy-six male Wistar rats were randomly divided into 2 groups ( n = 38): the CCI group which received the chronic constriction injury and the sham group which received the sham operation as control. The mechanical and thermal nociceptive thresholds were assessed with paw withdrawal latency (PWL) to von Frey filaments and radiant heat at 1d before and ld,4d,7d,14d and 28d after CCI operation. Five animals were sacrificed at each time point for real-time polymerase chain reaction (real-time PCR) and another three animals sacrificed at 7d postoperation for immunofluorescence histochemical staining. Results The thresholds to mechanical and thermal stimuli decreased obviously after operation in CCI group. The expressions of TNF-α and NF-κB mRNA began to increase at ld( (2.079 ±0. 104)times and 4d( ( 1.640 ± 0.064) times) after operation and reached the peak at 7d ((2.748 ±0.147)times, (2.010 ±0.096)times) ,then the expressions of TNF-a mRNA began to decrease,while the expressions of NF-kB mRNA maintained at a high level throughout the experiment. The result of immunofluorescence histochemical staining revealed that NF-kB and TNF-α protein expressions at 7 day increased significantly on the hippocampus,which was consisted with NF-κB and TNF-a mRNA levels. Conclusion The activation NF-κB and TNF-α in hippocampus may be involved in the procession of neuropathic pain.

Objective To explore the characteristics of polysomnography (PSG) of depressed patients and the correlation between rapid eye movement (REM) and severity degree of depression. Methods Polysomnography was used to assess patients'sleep condition and Montgomery-Asberg depression scale (MADRS) was used to assess the severity degree of depression. 90 patients and 30 healthy controls were included. Results Compared to healthy controls,sleep progress of depressed patients changed as follow:prolonged sleep latency((25.2 ±15.25) minutes) ,lowered sleep efficiency(0.853 ±0.11) ;the architecture of sleep also changed:percentage of stage 1 increased( (27.7 ± 16.38) % ),percentage of REM sleep increased( (22. 8 ± 6. 1 ) % ) , percentage of stage 2 decreased ((40.2±11.3)%), percentage of slow wave sleep decreased ((11.8 ±9. 32)%); REM sleep significantly changed; decreased REM latency((79. 27 ±30. 44) minutes) , increased REM activity((129. 0 ±53. 12) u) .increased intensity of REM((36.7 ±14.0)u/min), increased REM density((159.2 ±57.2)u/min) were observed in depressed patients. There was no obvious correlation between the variance of REM and severity degree of depression. Conclusion There are a series of changes in sleep progress, architecture and REM sleep of depression and the change of REM sleep can be specified to diagnose depression. However,there is no causality between REM variance and severity of depression.