| IntroductionDepression is the most popular kind of psychical disease. In recent years, there is growing evidence that pathophysiology of depression is associated with impairments of neuronal plasticity and cellular resilience. The damage of hipp-ocampal neuron is the important part in plasticity regulation of synapse and play a critical role in the mechanism of depression. Chronic stress can cause damage to brain, especially to the structure and the function of hippocampus, ultimately leads to the onset of depression. Glycogen synthase kinase 3β ( GSK - 3 β) is highly expressed in brain, modulates several signaling pathways concerned with neuronal plasticity, and is a key part of many regulations including neuronal plasticity and cell resilience. This study observes the effects of chronic stress on the expression of GSK - 3β, to discuss the mechanisms of brain damage and neuron protection in depression causing by chronic stress.Materials1. Animals: Forty — eight male young wistar rats.2. Reagents: Rabbit anti GSK -3β antibody ( Sigma);Goat anti rabbit SABC Kits (Beijing Zhongshan Co. );3. Apparatus: YSD -4 electronic stimulus instrument, Meta Morph/Cool Snapfx/Ax70 computer image analysis system.Methods1. According to Open - field, forty - eight rats were randomly divided intothe experimental group and the control group ,24 rats respectively.2. The experimental group rats randomly accepted different stimulus for 21 days to get depressive model rats, and all rats were taken Open - field test again on the 22ed day.3. The expression of GSK - 3 (3 in rat hippocampus were detected by western blotting.Results1. The weight and the numbers of field segments entered of experimental group were obviously lower then the control group.2. Compared to control group, the expression of GSK -3f$ in experimental group was increased( P < 0.05 ).Conclusion1. Chronic stresses cause rats losing weight and decrease the research -and - modify behaviors.2. Compared to control group, the expression of GSK -3(3 in experimental group was increased.3. GSK - 3 jB is possibly involved in the pathophysiology of depression including the alterations of neuroplasticity. The factors or methods that can regulate the expression of GSK - 3 fi may improve neuron survival and recovery ability , which develops a new way for the etiopathogenisis and the clinical therapy of depression. |
