| Aim：Establishing a chronic unpredictable mild stress rats model, this study aim to explore1.whether there was a recovery of impairment in learning and memory in rats after the undock ofstressorschronic stress2.the effect of chronic stress on GFAP and EAAT2protein expression inhippocampal astrocytes3.under the condition of chronic stress whether there was a differentexpression of protein GFAP and EAAT2in three areas of hippocampus4.focus on possibleasymmetrical expression of GFAP and EAAT2under chronic stress in rat hippocampal astrogliaand then confirmedthe conclusion in our past study that chronic stress caused right-deviationimpairment in hippocampus5.to further explore the repair mechanism of hippocampal damageand find the answer whether expression of GFAP and EAAT2protein returned to normal levelwhen stressors were removed.Methods:Normal Male Sprague-Dawley were randomly divided into control group, chronicstress group and recovery groupusing5weeks chronic unpredictable mild stress (CUMS)methods to set up the rat model of chronic stress and then gave a35-day recovery phase.Learning and memory ability of each group were evaluated by Open field test, Morris watermaze and "Y" maze. After the behavior tests, further study on bilateral hippocampal astrogliawere observed by the expressions of protein GFAP and EAAT2in hippocampus analyzed withwestern blot. Then a method of immunohistochemistry was used to examine the possibleasymmetric expression of the two proteins in three subregions of hippocampus while observedwhether all these changes could be reversed.Results：1.Chronic stress impact on hippocampal function and after the undock of stressorsthere was a degree of recovery. In Morris water maze, rats in recovery group presented asignificant lower latency(P<0.01) than chronic stress and control group on learning phase, and ontesting phase these rats also showed a longer time spent in objective quadrant（P<0.05）. In "Y"maze, chronic stress group had no preference in novel arm while in recovery group and controlgroup rats appeared a higher percentage of shuttling frequency.2. In the experiment of western blot, compared to control group, stress group showed a significant up-regulated in GFAP proteinexpression（P<0.05） and a down-regulated in EAAT2protein expression（P<0.05）.3.Theobvious alteration of GFAP and EAAT2protein expression was found in CA1and CA3areaasymmetric impact of chronic stress on hippocampal astroglia: In western blot experiment,chronic stress group showed an up-regulated expression of GFAP and a down-regulatedexpression of EAAT2in hippocampus without an asymmetric change. Inimmunohistochemistry,there were no significant change in bilateral DG area of hippocampus. InCA3area right hippocampus showed a significantly increased expression of GFAP in thecondition of chronic stress without a decrease after recovery, while the similar increasing in lefthippocampi were reserved after stressors removed. In the expression of EAAT2protein, chronicstress group revealed a significant decrease especially in right side while an up-regulated wasviewed in recovery group. In CA1area, alteration of GFAP expression was as similar as CA3area except that there was no significance while in EAAT2protein all groups showed a higherexpression in the left side than right.Conclusion： We conclude that1.Chronic stress can trigger functional impairments inhippocampus of male rats and there was a recovery alteration when stressors was moved for35days.2.Meanwhile, chronic stress showed an asymmetry impact on hippocampal astrocytes. Itturned out to be higher sensibility to chronic stress in CA3area. After thirty-five days of stressorelimination, although there was a partial reverse of astroglia alterations, it still could not go backto the normal level. |
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