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Chronic stress on rat brain NMDAR1 protein expression and NO Content

Author: ChenQiaoZhen
Tutor: LiHuiChun
School: Zhejiang University
Course: Psychiatry and Mental Health
Keywords: Chronic mild stress Sprague-Dawley rat Depression Prefrontal cortex Hippocampus Nitric oxide N-methyl-D-aspartate receptor
CLC: R749.4
Type: Master's thesis
Year: 2004
Downloads: 171
Quote: 2
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Abstract

Background Depression cause is unknown, with high morbidity and recurrence rates, and to the community to bring a heavy burden of disease. Existing slower onset of antidepressant drugs, limited efficacy; Moreover, some drugs on the mechanism of action of neurotransmitters can produce the opposite but equally antidepressant effect, these clinical paradox difficult monoamine theory to explain. In recent years, researchers have made a lot of use of various models of depression and mental pharmacological relevant neurobiological research. Stress and depression onset Given the close relationship between stress model in the pathogenesis of depression and antidepressants screening application of the most common. More and more evidence that the incidence of depression and the mechanism of action of antidepressant drugs quite complex, involving a variety of substances and pathways in brain abnormalities, but have yet to find the final path. Glutamate is the major excitatory brain neurotransmitter Numerous studies have shown that the passage of N-methyl-D-aspartic acid (N-Methyl-D-Aspartate, NMDA) receptors involved in the excitability synaptic transmission, neural plasticity, neural development and aging, learning and memory and other important physiological processes. Currently, the role of glutamate excitotoxicity is also considered with some neuropsychiatric diseases such as cerebrovascular disease, trauma, epilepsy, schizophrenia pathogenesis-related. NMDA receptors and anxiety about depression study less, but in vitro experiments have prompted some antidepressants can directly block the NMDA receptor pathway and nitric oxide synthase (Nitric oxide synthesis, NOS) expression and activity; while Some NMDA receptor antagonists or NOS inhibition Zhejiang Lee Master Thesis agents may have a similar antidepressant effect. For chronic stress model of depression brain NMDA receptor subunit NRI main expression has not been reported at home and abroad. Aim of the present study was to use and sub-chronic mild stress model of raising a combination of two classic, the use of long-term unpredictability to establish mild stress rat model of depression, combined with rat body weight and behavior changes, respectively spectrophotometry and immunoblotting depression rat prefrontal cortex, hippocampus nitric oxide (Nitricox remember e, NO) content and the NMDA receptor subunit Lord (NRI) expression changes, designed to reveal the chronic stress on the valley histidine an NMDA receptor an NO pathway, and to explore the possible mechanism of depression, as antidepressant research and development to provide clues. Methods 16 adult male SPrague an Dawley rats were randomly divided into control and chronic stress model group, using transform rearing environment, circadian rhythm and adjust your diet and water and other chronic unpredictable mild stress rat depression model to body weight and behavioral changes to ensure the reliability of the model. In establishing model based on the spectrophotometric detection of rat prefrontal cortex and hippocampus NO content changes; Western blot analysis of the expression of the corresponding brain areas NRI case. Results 1 model rats slow weight gain, decreased activity, loss of interest, successfully simulated the antipsychotic clinical depression symptoms. To modeling the end of the control group and model group were weight gain (128.19 ± 18.22) g and (80.75 ± 13.38) g, the difference was significant between the two groups was statistically significant (P = 0.OOO); in open box experiment, rats, activity levels (22.62 ± 12.26) was significantly less than the control group (43.75 ± 19.88), the difference was statistically significant (P = 0.023): the model group rats before and after stress were absolutely sucrose consumption is (82.31 Shi 10.08) g and (70.81 Shi 13.59) g, which is less than the former, but the difference did not reach statistical significance retaining dagger 0.060), and the corresponding relative sucrose consumption (absolute amount / weight) were (0.28 Guests, 0.03) and (0.19 ± 0.04), the difference was statistically significant (P = 0.001). (2) Long-term mild stress, the prefrontal cortex and hippocampus of NO levels were significantly increased in the control group and model group rats prefrontal area No content was (26.97 ± 1 .38) runoUmg · pro and (31.00 Guests 2.55) father Zhejiang University master's degree thesis nmoUmg · pro (P = 0.0o2), corresponding hippocampus NO levels were (36.06 ± 0.87) nmo flail g · pro and (38.11 ± 1.73) nlno decorated g.pro (P = 0.010). Correlation analysis showed that depression model NO content in hippocampus of rats with spontaneous activity was negatively correlated (: twenty-one 0.755, corpse two .031). 3 Western blot analysis showed that chronic stress may increase the expression of NRI hippocampus (P = 0.004), while the prefrontal region NRI expression has not yet seen a significant change (for .659). NRI depression rat hippocampus expression correlated with the amount of activity (r = a 0.719, corpse = 0.045). Conclusions 1. Study of chronic mild stress and raising two classic model combines the use of long-term unpredictability of mild stress, the successful establishment of a more ideal animal model of depression, which for the in-depth study provides experimental pathogenesis of depression platform. 2 chronic stress can promote the prefrontal, hippocampus NO synthesis; while increasing the expression of hippocampus NRI; hippocampus of rats these changes and spontaneous activity are closely related. The results suggest that specific parts of the brain NO content and NRI subunit protein plasticity may be involved in chronic stress model of depression in rats during the occurrence of the NMDA receptor an intervention will be NO pathway antidepressants development and clinical depression disease treatment to provide new ideas.

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