| PrefaceDepression is the most popular kind of psychical disease. It has a higher recurrent rate and lifetime morbidity. There is growing evidence from neuroimag-ing and postmortem studies that severe mood disorders, which have traditionally been conceptualized as neurochemical disorders, are associated with impairments of structural plasticity and cellular resilience. The damage of hippocampal neuron is the key 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. In this course, the disfunction of many neuron protective mechanisms is very important. Heat shock protein 70 ( Hsp70) is one of stress proteins that induced by stress stimulus, which can protect neuron from stress. This study observes the effects of chronic unpredictable stress on the levels of Hsp70 expression, to discuss the mechanisms of brain damage and neuron protection in depression causing by chronic stress.Materials1. Animals: Fifty male young wistar rats.2. Reagents: Rabbit anti heat - shock protein70 monoclonal antibody ( Santa Cruz Co. ) ; Goat anti rabbit Streptavidin/Peroxidase Histostain? - Plus Kits ( Beijing Zhongshan Co. ) ;DAB Kits( Beijing Zhongshan Co. ).3. Apparatus; YSD -4 electronic stimulus instrument, Meta Morph/CoolSnapfx/Ax70 computer image analysis system.Methods1. According to Open -field, fifty rats were randomly divided into the experimental group (EG, 25rats) and the control group (CG, 25 rats). Then the experimental group and the control group were singly divided into five group (5rats in each group) according to the moments after acute forced - swimming2. 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. On the 23ed day, all rats were taken forced swimming one by one for 5 minutes.4. The Hsp70 in different regions of rat hippocampus were detected by im-munohistochemistry of special antibody at 2h,4h,6h,18h,24h and 48h after a-cute forced - swimming.ResultsThe weight and the numbers of field segments entered of experimental group were obviously lower then the control group.Compared to control group, the expression of Hsp70 in depression rats after acute forced - swimming stress in hippocampus CA3 region and dentate gyrus was significantly decreased( P < 0.05 ).DiscussionThis study use chronic unpredictable stress of middle intension to make depressive model rats. According to the results of Open - field test, the weight and the activity of experimental group were obviously lower then the control group, so the model is successful.Heat shock protein 70(Hsp70) , can combine and degradation the apomor-phosis proteins, and promote the recover of the normal protein syntheses, inhibit the cell apoptosis, thus to protect the cell from the damage of harmful stimulus. In normal condition, Hsp70 only small amounts expresses, and the synthese of Hsp70 increases significantly to adapt the intension of stress. In this study, there isnt obvious difference between the amounts of Hsp70 in hippocampus of two groups after 2 hours of forced - swimming; ever since 6 hours after forced -swimming, the Hsp70 expression of experimental group is always lower than the control group. The ability that the hippocampus of experimental rats synthesize Hsp70 degrades, which impairs the endurance against impairment, one of the possible reasons is that chronic stress cause the disturbance of structure and function in hippocampus.Chronic stress induce the disturbance of neuron structure and function, which can enable the intracellular signaling pathway, thus promote the expression of Hsp70 to lower the neuron damage caused by harmful stimulus. If the stress exist continually, the level of Hsp70 that neurons synthesize drops and can t adapt the stress intension, which is one of the possible signs to the descend of neuronal activity.Traditional anti - depression therapy mainly aims at the disturbance of neurotransmitters. To promote neuron protective mechanisms, and to improve neuron survival and recover ability, develops a new way for the etiopathogenisis and the clinical therapy of depression.Conclusion1. Chronic composite stresses cause rats losing weight and decrease the research and modify behaviors.2. Compared to control group, the expression of Hsp70 in chronic stress rats after acute forced - swimming stress in hippocampus CA3 region and dentate gyrus was significantly decreased.3. Under chronic stress condition the ability that neuron synthesize Hsp70 degrades, which is one of the possible signs to the descent of neuronal activity. |
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