| Summary: | 碩士 === 輔仁大學 === 臨床心理學系碩士班 === 103 === The core system of major depression is depressive mood and anhedonia. Moreover, the depressive symptoms of the patients’ complain in the clinic also include the impaired cognitive function, such as memory loss, attention deficit and so on. The previous research found that rats after chronic mild stress(CMS) cause memory loss, as well as relate to excessive dopamine in the medial prefrontal cortex(mPFC). Furthermore, some researches point that excessive dopamine may decrease the phosphorylation of Erk1/2 in the downstream of the cell signaling. Therefore, understanding the memory function and the neurochemistry mechanism of depression can help to offer the clinical evidence in the psychopathology of major depression.
The main purpose of the research is to investigate the changes of neurotransmitter in the mPFC and hippocampus CA3 whether affecting memory through CMS animal model imitating depression. We use the object recognition test (ORT) and object location test (OLT) to evaluate the rat's memory performance as well as to test the rat's performance of multiple behavior. Then, we use microdialysis to test whether there are changes in the dopamine and the serotonin in the mPFC and hippocampus CA3 of the CMS rats. At the last, we use the immunohistochemical staining to test the changes of the Erk1/2 in the mPFC and hippocampus CA3. Moreover, we test the relationship between dopamine system and ERK 1/2 by intraperitoneal injection of dopamine type II-receptor antagonist. Therefore, there are three hypothesis of the research: 1) the CMS rats could cause the memory loss; 2) the CMS rats could cause the abnormal secretion of dopamine and serotonin in the mPFC and hippocampus CA3, as well as cause the abnormal activity of Erk1/2. 3) After the intraperitoneal injection of dopamine type II-receptor antagonist, the abnormal activity of ERK1/2 in CMS rats can be reversed.
The results of the research show that CMS rats have the symptoms of anhedonia and decreased activity. Moreover, the object recognition memory and object location memory are obviously impaired. According to the analysis of neurotransmitters, it shows that after treating 100mM KCL to the CMS rats, the releasing percentage of the dopamine in mPFC and CA3 is obviously increasing. However, there are no significant difference in serotonin in mPFC and CA3. Moreover, the number of cells in the expression of pERK in granule layer and pyramidal layer of hippocampus and in mPFC of CMS rats are significant decreasing, but the number of cells in expression of pERK in other regions of hippocampal are significant increasing; however, the intraperitoneal injection of dopamine type II-receptor antagonist to the CMS rats can reverse the above results. However, we need to start a further research to clarify the relationship among the high concentration of dopamine releasing in mPFC and hippocampal, the abnormal brain regions of pERK and cognitive decline
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