8-OH-DPAT对青春期病理性攻击大鼠前额叶皮层和海马内BDNF及GDNF的影响
发布时间：2018-10-05 10:14
【摘要】：目的探索8-OH-DPAT即五羟色胺(5-HT)1A受体激动剂对青春期病理性攻击大鼠前额叶皮层、海马内脑源性神经营养因子(BDNF)和胶质源性神经营养因子(GDNF)的影响,为进一步探索病理性攻击行为的生物学机制提供一定基础。方法1实验动物及分组购买雄性Sprague-Dawley(SD)大鼠56只(购于重庆医科大学实验动物中心,生后21天),随机分成6组:实验组(即模型组,n=7)、对照组(即空白对照组,n=7)、实验药物组(n=7)、实验盐水组(n=7)、对照药物组(n=7)、对照盐水组(n=7),剩余大鼠为入侵鼠(工具鼠)(n=14)。2青春期病理性攻击大鼠模型建立及攻击、神经营养因子检测从出生后21天开始,对实验组、实验药物组及实验盐水组均采用国际通用早年慢性应激方法建立病理性攻击大鼠模型,应激手段主要有孤养、昼夜颠倒、去奖赏挫败、预激惹刺激和居住-入侵实验,至出生后56天即青春期结束应激。对照组、对照药物组、对照盐水组及入侵鼠均正常养育。建模完成后对上述6组采用居住-入侵实验行攻击行为检测,检测指标包括攻击潜伏期、攻击要害部位、屈服后继续攻击。完成攻击行为检测后对实验组、对照组断头取前额叶皮层、海马行免疫印迹检测BDNF、GDNF蛋白水平。3 8-OH-DPAT干预后攻击、神经营养因子检测对实验药物组、对照药物组腹腔注射两周的8-OH-DPAT(0.5mg/kg),对实验盐水组、对照盐水组腹腔注射两周的生理盐水(2ml/只)。攻击、神经营养因子检测方法及指标同前。结果1成功建模后攻击、神经营养因子检测1.1攻击行为:实验组与对照组比较,实验组攻击潜伏期显著缩短,差异有统计学意义(P0.01);实验组攻击要害部位和屈服后继续攻击显著增加,差异具统计学意义(P0.01)。1.2神经营养因子:免疫印迹检测发现:实验组大鼠前额叶皮层BDNF、GDNF蛋白较对照组降低,差异有统计学意义(P0.01)。对于海马内BDNF及GDNF蛋白,实验组亦较对照组降低,差异有统计学意义(P0.01)。2干预后攻击、神经营养因子检测2.1干预后攻击行为比较:2.1.1攻击潜伏期:8-OH-DPAT干预后的实验药物组与实验盐水组相比,实验药物组大鼠攻击潜伏期延长,差异具统计学意义(P0.05),而实验盐水组与对照盐水组、实验药物组与对照药物组、对照药物组与对照盐水组之间比较,差异均无统计学意义(P0.05)。2.1.2攻击要害部位:实验药物组较实验盐水组明显减少(P0.01),实验盐水组与对照盐水组、实验药物组与对照药物组、对照药物组与对照盐水组之间相比,差异均无统计学意义(P0.05)。2.1.3屈服后继续攻击:实验盐水组较对照盐水组仍显著增加(P0.01)、实验药物组较实验盐水组显著降低(P0.01),对照药物与对照盐水组、实验药物与对照药物比较,差异均无统计学意义(P0.05)。2.2干预后大鼠前额叶皮层和海马内神经营养因子检测2.2.1前额叶皮层:实验盐水组大鼠前额叶皮层内BDNF、GDNF蛋白水平较对照盐水组显著降低(P0.01,P0.05),实验药物组较实验盐水组显著增加(P0.01,P0.05)。对照药物与对照盐水、实验药物组与对照药物组相比,差异无统计学意义(P0.05)。2.2.2海马:对于海马内BDNF、GDNF蛋白,实验盐水组较对照盐水组显著降低(P0.01),实验药物组较实验盐水组增加,差异具统计学意义(P0.01)。对照药物组与对照盐水组、实验药物组与对照药物组相比,差异无统计学意义(P0.05)。结论1青春期大鼠经历早年慢性应激后可产生病理性攻击。2经历早年慢性应激后的青春期大鼠前额叶皮层及海马内的BDNF、GDNF蛋白水平降低,可能是其产生病理性攻击行为的因子。3 5-HT1A受体激动剂,即8-OH-DPAT可上调前额叶皮层和海马内的BDNF、GDNF蛋白,并可在一定程度上减轻青春期大鼠的由早年慢性应激引起的病理性攻击行为。
[Abstract]:Objective To explore the effect of 8-OH-DPAT (5-HT) 1A receptor agonist on the prefrontal cortex, the brain-derived neurotrophic factor (BDNF) and glial source neurotrophic factor (NPY) in the rat prefrontal cortex and hippocampus. It provides a foundation for further exploring the biological mechanism of pathological attack. Methods56 male Sprague-Dawley (SD) rats were randomly divided into 6 groups: experimental group (model group, n = 7), control group (control group, n = 7) and experimental group (n = 7). The experimental saline group (n = 7), control group (n = 7), control saline group (n = 7), the remaining rats were invading rat (tool rat) (n = 14). The experimental drug group and the experimental saline group were used to establish the pathological attack rat model by using the international general early-age chronic stress method, and the stress method was mainly solitary, day-and-night upside down, dereward frustration, pre-excitation stimulation and residence-invasion experiment, and the stress was terminated at 56 days after birth, that is, puberty. Control group, control group, control saline group and invasive mice were all normal. After the modeling is finished, the 6 groups are detected by the residential-intrusion experiment line attack, and the detection indexes include the attack latency, the attack key position and the yield, and then the attack is continued. The experimental group and the control group were divided into two groups: 8-OH-DPAT (0. 5mg/ kg), which was injected intraperitoneally with 8-OH-DPAT (0. 5mg/ kg). The control saline group was injected into the abdominal cavity for two weeks of normal saline (2ml/ only). and the detection method and the index of the attack and the neurotrophic factor are the same. Results 1. The attack latency of the experimental group was significantly shortened and the difference was statistically significant (P0.01). The difference was statistically significant (P 0.01). 1. 2 neurotrophic factor: The experimental group was found to have a statistically significant difference in BDNF and p27 protein in the prefrontal cortex of the experimental group (P0.01). Compared with the control group, there was statistical significance in the experimental group (P0.01). After the intervention, the nerve nutrition factor was detected by 2.1. The attack latency: 8-OH-DPAT intervention group was compared with the experimental saline group. In the experimental group, the latency of attack was prolonged and the difference was statistically significant (P0.05). The experimental saline group and the control saline group, the control group and the control group were not statistically significant (P0.05). Compared with the control saline group, there was no significant difference between the control group and the control saline group (P0.05). Compared with the control saline group, the saline group of the experimental group was significantly lower than that in the control saline group (P0.01). Compared with the control saline group, the experimental drug was compared with the control saline group. There was no statistical significance in the difference (P 0.05). 2. 2. The levels of BDNF and NPY in the prefrontal cortex of the experimental saline group were significantly lower than that in the control saline group (P <0.01, P 0.05). The experimental group was significantly higher than that in the saline group (P <0.01, P 0.05). Compared with the control saline group, the difference was not statistically significant (P0.05). The difference was statistically significant (P0.01). Compared with the control group, there was no significant difference between the control group and the control group (P0.05). Conclusion The level of BDNF and tau protein in the prefrontal cortex and hippocampus of adolescent rats after chronic stress in the early years may be a factor of pathological attack. The 5-HT1A receptor agonist, That is, 8-OH-DPAT can upregulate BDNF and p27 protein in the frontal cortex and hippocampus, and can reduce the pathological behavior induced by chronic stress in the early years of puberty.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R749
本文编号：2252999
[Abstract]:Objective To explore the effect of 8-OH-DPAT (5-HT) 1A receptor agonist on the prefrontal cortex, the brain-derived neurotrophic factor (BDNF) and glial source neurotrophic factor (NPY) in the rat prefrontal cortex and hippocampus. It provides a foundation for further exploring the biological mechanism of pathological attack. Methods56 male Sprague-Dawley (SD) rats were randomly divided into 6 groups: experimental group (model group, n = 7), control group (control group, n = 7) and experimental group (n = 7). The experimental saline group (n = 7), control group (n = 7), control saline group (n = 7), the remaining rats were invading rat (tool rat) (n = 14). The experimental drug group and the experimental saline group were used to establish the pathological attack rat model by using the international general early-age chronic stress method, and the stress method was mainly solitary, day-and-night upside down, dereward frustration, pre-excitation stimulation and residence-invasion experiment, and the stress was terminated at 56 days after birth, that is, puberty. Control group, control group, control saline group and invasive mice were all normal. After the modeling is finished, the 6 groups are detected by the residential-intrusion experiment line attack, and the detection indexes include the attack latency, the attack key position and the yield, and then the attack is continued. The experimental group and the control group were divided into two groups: 8-OH-DPAT (0. 5mg/ kg), which was injected intraperitoneally with 8-OH-DPAT (0. 5mg/ kg). The control saline group was injected into the abdominal cavity for two weeks of normal saline (2ml/ only). and the detection method and the index of the attack and the neurotrophic factor are the same. Results 1. The attack latency of the experimental group was significantly shortened and the difference was statistically significant (P0.01). The difference was statistically significant (P 0.01). 1. 2 neurotrophic factor: The experimental group was found to have a statistically significant difference in BDNF and p27 protein in the prefrontal cortex of the experimental group (P0.01). Compared with the control group, there was statistical significance in the experimental group (P0.01). After the intervention, the nerve nutrition factor was detected by 2.1. The attack latency: 8-OH-DPAT intervention group was compared with the experimental saline group. In the experimental group, the latency of attack was prolonged and the difference was statistically significant (P0.05). The experimental saline group and the control saline group, the control group and the control group were not statistically significant (P0.05). Compared with the control saline group, there was no significant difference between the control group and the control saline group (P0.05). Compared with the control saline group, the saline group of the experimental group was significantly lower than that in the control saline group (P0.01). Compared with the control saline group, the experimental drug was compared with the control saline group. There was no statistical significance in the difference (P 0.05). 2. 2. The levels of BDNF and NPY in the prefrontal cortex of the experimental saline group were significantly lower than that in the control saline group (P <0.01, P 0.05). The experimental group was significantly higher than that in the saline group (P <0.01, P 0.05). Compared with the control saline group, the difference was not statistically significant (P0.05). The difference was statistically significant (P0.01). Compared with the control group, there was no significant difference between the control group and the control group (P0.05). Conclusion The level of BDNF and tau protein in the prefrontal cortex and hippocampus of adolescent rats after chronic stress in the early years may be a factor of pathological attack. The 5-HT1A receptor agonist, That is, 8-OH-DPAT can upregulate BDNF and p27 protein in the frontal cortex and hippocampus, and can reduce the pathological behavior induced by chronic stress in the early years of puberty.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R749
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