| PrefaceDepression is the main form of feeling disorders, endangering mankind's body and mental health . It is a main mind problem of the whole world , occuring commonly and frequently . Depression recurs obviously , and tends to chronici-zation . Its suiside rate is make an appointment with 10% - 15% and the prognosis is most incorrect well . More and more observations suggested that depression is not a completely functional mental disorder, at least, considerable part of it has been found structural changes in brain . Life event especially chronic un-predicted stress play an important role in depression. Chronic stress induced series of physiological and biochemical changes in the organism , especially activation HPA so that GC secreted excessively, and arouse much more GC in blood. Chronic stress made the damage of neural structure and function in hippocampus and it maybe has relationship with many kinds of mental diseases such as PTSD and depression . The treatment of depression should 'not only aim at nerve transmit ee'j but also consider to protect neurons. Decreasing the neural injury and protecting the brain from being damaged should be a new and important target for the treatment of depression.The mechanism of chronic stress injury hippocampus is not fully clear, but with the development of the nervebiology, it will be a issue to study the pattern of nerve activation from gene and molecule level. IEG consist of closely hundred members including c - fos , c-jun and at the moment c - fos , c-jun have been studied deeply.In the past few years ,c-fos ,c-jun have been served as an important method in studying brain injury induced by stress and the expression of FOS, JUN could be used as a marker to follow the functional activity of neurons. So in the present study, we used the expression of c-jun as the marker indicating the neu-ral activity in the hippocampus of rats being exposed to unpredicted chronic stress to study the relation between the expression of c-jun and the structural and functional changes in the hippocampus. This would help to study the pathogene-sis of depression, and would provide basis for the treatment of depression.MaterialsExperimental animals: Male Wistar rats ( n = 36 ) weighting about 200 -300g were purchased from the center of experimental animals in China Medical Univercity.Experimental reagents: Rabbit anti - c-jun and SABC kit ( Boster Biotechnology Co. LTD. )Experimental instruments: Electrophysiological apparatus, Meta Morph/ Cool Snapfx/AxVO image analysis system.MethodsExperimental rats were housed for 7 days to adapt the conditions of the lab. After that, they were divided into 2 groups (n = 18/group) randomly on the basis of their weights and the results of Open - field test.The rats in group A were exposed to forced - swimming stress on the 22" day only. The rats in group C were exposed to chronic stress conditions. They received various types of stresses everyday for consecutive 21 days followed by a forced swimming stress on the 22nd day. Open - field tests were carried on each rat before the last stress.0min, 30min, Ih, 3h, 5h, 8h after the beginning of the last swimming stress, 3 rats were selected from each group to be anaesthetized with 69mg/kg (i. p. ) of sodiumpentobarbital and perfused via left ventricle with 200ml saline followed by 300ml 4% paraformaldhyde. Brains were removed and postfixed for more than 48 h. Then the brains were dehydrated through graded - concentration ethanol and embedded in olefin. And sections were cut coronally.Immunohistochemistry method was used to measure the expression of JUNprotein in the hippocampus. 5 pieces of hippocampal sections of every rat were analysed on image analysis system. One - way ANOVA was used to comoare the differences in the expression of JUN between each group or between each time point of a group with spss 11.0 statistic software.Results1. Neurons under light microscopeCompared with group A, the distance between CA3 pyramidal neurons increased and the amo... |
PDF Full Text Request