The Expression Of Galanin And Galanin Receptor-2 In The Brian Of Chronic Stress Model Of Depression

Depression is a mind disorder which can cause acute variety of emotion and bad temper. The neurobiological mechanism of depression hasn' t been learned clearly till now. But the mental injury caused by long time pressure or sudden events was considered as the major causation of depression. Hippocampus is a main structure taking part in the stress reaction. The message of stress acts first on hippocampus, then arouse the activity of efferent nerves of hippocampus, which simultaneously arouse the excretion of hypothalamus CRF and enhance the function of hypotha-lamic-pituitary-adrenal axis (HPA axis). Clinically, most depression patients come through the process of rapid or chronic stress. The theory that stress brings on the enhancement of (HPA) , then causes the decline of monoamine transmitters system and results in depression is the major hypothesis for depression.Since Tatemoto isolated galanin(GAL) from pig' s small intestine in 1983, scientists have done a lot of research of its function. GAL possesses a wide distribution in central and peripheral nervous system, and take part in modulation of many physical functions such as sex and procreation, learning and memory, pain, neuroendocrene and so on. Along with the broad use of immunohistochemistry and in situ hybridization, scientists found the expression of GAL and its receptors increase evidently in Alzheimers disease and depression patients. High expression of GAL and its receptors also occur in injured areas of nervous system. The results show that GAL probably participating in neurodegeneration and neuroregeneration.In this study, we adopted a chronic stress rat model of depression and estimate the model with open-field test to observe their behavior reaction and with HPLC to analysis the blood serum cortisol to evaluate the function of HPA axis. The changes of monoamine transmitters from different areas in rat brain were tested by HPLC method. The in situ hybridization, immunohistochemistry andRT-PCR were used for further research of expression of GAL and its receptors. The locomotion activity extremely reduced after chronic stress but the level of serum cortisol increased evidently. The expression of GAL and its receptor-2 in hippocampus and dorsal raphe nucleus increased obviously. The high expression of galanin and galanin receptor-2 in some brain area suggested that galanin probably take part in the modulation of the function of neurons during the stress process. This study is aimed at learning the relationship between expression of GAL and the function of neurons in hippocampus and dorsal raphe nucleus. It is important for further study of pathology and physiology of depression and is valuable for searching the antidepressant new compounds.