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Chronic stress depression in hippocampal neuropeptide Y and nitric oxide synthase relationship

Author: LianZuo
Tutor: AnShuCheng
School: Shaanxi Normal University
Course: Physiology
Keywords: Depression Hippocampal Chronic unpredictable stress NPY NOS
CLC: R749.4
Type: Master's thesis
Year: 2010
Downloads: 134
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Abstract

The depression is caused by a variety of reasons, depressed mood (depression) is one of the main symptoms of mood disorders (mood disorder). With social competition and pressure of living increases, the incidence of depression (depression) is rising, by the widespread concern about depression causes, mechanisms and prevention strategies. Previous studies have proposed that the occurrence of depression and chronic stress. However, the precise pathological mechanisms of stress-induced depression remains unclear. Recent research suggests that the hippocampus (hippocampus) is the target site of stress hormones, it is not only high regulation center of the stress response by stress involving the most sensitive area, and is closely related with the occurrence of stress-induced depression. With the gradual deepening of the mechanism of depression, neuropeptide Y, because of their emotional and behavioral stress reactions play an important role and has caused widespread concern, hippocampal NPY is generally believed that by protecting neurons play an antidepressant effect, however, about NPY antidepressant effect or NPY to reduce the lead to depression is still unclear through what channels. NO as an atypical nerve messenger concern in recent years. Some studies have shown that the NOS and depression are closely related, NO release excess lead to damage of hippocampal neurons may play an important role in the pathogenesis of depression. NOS, including neuronal NOS (neuronal nitric oxide synthase, nNOS), endothelial NOS (endothelial nitric oxide synthase, eNOS) and inducible NOS (inducible nitric oxide synthase, iNOS) three kinds nNOS and iNOS produces excessive NO The neurotoxin role. Reported in the literature of BDNF and Kalirin-7 and other anti-depressants and protect neurons by inhibiting NOS achieve. Chronic unpredictable mild stress may be excessive release glutamate, NMDA receptor over-activation, inhibit NPY expression, resulting in depression. Glutamate overactivation of NMDA receptors caused depression-like behavior and hippocampal NOS expression elevated. Accordingly, we speculated, NPY may also play an antidepressant effect by inhibiting NOS. In this study, through the establishment of chronic mild unpredictable stress (chronic unexpected mild stress, CUMS) model of depression, Microinjection of NPY and NPY-Y1 receptor blocking, NOS inhibitors, measuring animal body weight change sucrose preference open box test and forced swimming test behavior test combined with immunohistochemical methods to detect nitric oxide synthase (nitric oxide synthase, NOS) including NPY, neuronal NOS and inducible NOS expression changes in hippocampus of chronic should The shock of depression in hippocampal NPY and NOS relationship. The results are as follows: 1 control rats (n = 8) compared to moderate chronic unpredictable stress (Chronic unpredicted mild stress, CUMS) rats (n = 10) weight downward trend; showed obvious depression-like behavior changes; with hippocampal NPY decreased expression of the iNOS and nNOS expression was significantly increased. 2 of NPY in CUMS rats (n = 9) weight upward trend; hippocampus microinjection of NPY can significantly improve the performance of stress-induced depression-like behavior in rats; reduce hippocampal expression of NOS. NPY-Y1 receptor selectively block the body weight of the rats (n = 9) downward trend; behavioral performance of rats decreased ability; hippocampus iNOS and nNOS expression was elevated. 3. Hippocampal microinjection of NOS inhibitors reversed CUMS caused slow weight gain in rats and depression-like behavioral changes (n = 7). 4. Hippocampal microinjection of NOS inhibitors can reverse the decreased ability of the NPY-Y1 blockers cause weight loss in rats and behavioral performance (n = 10). In summary, in CUMS and hippocampal injection of NPY-Y1 receptor blockers can cause depression-like behavior performance hippocampal NOS expression is elevated. NPY high expression of NOS inhibition induced by stress, effectively improve the chronic stress-induced depression-like behavior. NOS blockers can be reversed the CUMS and hippocampal injection of NPY-Y1 blockers cause depression-like changes in behavior. Description chronic unpredictable stress caused NPY reduced NOS high expression, NO excessive production, may lead to damage of hippocampal neurons is one of the main reasons for the chronic stress depression. The occurrence of depression is very complex mechanism, through the regulation of the NPY-Y1 receptor, reduced NOS overexpression may be one important strategy for the treatment of depression. The NPY system can be used as a new pharmacological target for the treatment of stress-related depression and other mental illness.

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