| 李善华,周利,张霞,等.侧脑室注射鼠神经生长因子对阿尔茨海默病转基因模型小鼠学习能力及行为学的影响[J].安徽医药,2019,23(2):232-236. |
| 侧脑室注射鼠神经生长因子对阿尔茨海默病转基因模型小鼠学习能力及行为学的影响 |
| Effects of intracerebroventricular injection of nerve growth factor on learning abilities and behavior of transgenic mice with Alzheimer's disease |
| 投稿时间：2017-10-14 |
| DOI： |
| 中文关键词: 鼠神经生长因子 阿尔茨海默病转基因模型 脑源性神经营养因子 海马 膜电位 |
| 英文关键词: Mouse nerve growth factor Alzheimer's disease transgenic model Brain derived neurotrophic factor Hippocampus Membrane potential |
| 基金项目: |
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| 中文摘要: |
| 目的 探讨鼠神经生长因子(mNGF)侧脑室注射影响阿尔茨海默病(AD)转基因模型小鼠学习记忆能力及行为学的可能机制。方法 将20只老年痴呆转基因小鼠(C57BL/6J)采用随机数字表法分为AD转基因模型组(AD组)和实验组,每组10只小鼠,另取老年正常C57BL/6J小鼠10只设为老年组。AD组和实验组分3次(间隔10 d)侧脑室注射mNGF,老年组注射等量0.9％氯化钠注射液。用Morris水迷宫视频跟踪分析系统进行空间探索实验；采用全细胞膜片钳记录海马CA1区诱发的群峰电位(PS)和自发性动作电位(AP)；采用免疫组化法检测小鼠海马CA1区脑源性神经营养因子(BDNF)和神经生长因子(NGF)表达水平；实时定量聚合酶链式反应检测海马CA1区中BDNF mRNA和NGF mRNA水平。结果 治疗第40天,实验组小鼠脑薄片海马回CA1区BDNF[(100.51±2.27) ng/mL]和NGF[(159.85±1.23) ng/mL]蛋白阳性表达及BDNF mRNA[(72.02±0.98) β-actin]、NGF mRNA[(67.08±1.16) β-actin]明显升高,PS[(63.02±1.25) mV]和AP[(58.57±0.93) mV]膜电位降低,三组间的治疗前和第40天比较均差异有统计学意义(均P<0.05)。实验组小鼠跨越平台次数(4.29±0.64)明显高于AD组和治疗前同组[(2.85±0.12),(2.68±0.24)](F=49.815,232.391,P<0.05),实验组逃避潜伏期[(21.73±0.54)s]较AD组[(68.59±2.01)s]明显缩短,与AD组和治疗前同组比差异有统计学意义(F=2 910.165,3 137.281,P<0.05)。老年组运动轨迹主要在原平台位置,AD组则主要分散在外周,而实验组运动轨迹在两者之间。结论 鼠神经生长因子能促进AD转基因模型小鼠学习记忆能力,其作用机制可能与mNGF稳定海马CA1区膜电位,上调BDNF和NGF蛋白及其基因表达以营养和修复神经有关。 |
| 英文摘要: |
| Objective To investigate the possible mechanism of intracerebroventricular injection of mouse nerve growth factor (mNGF) on learning and memory abilities and behavior of transgenic mouse model with Alzheimer's disease.Methods Twenty senile dementia transgenic mice (C57BL/6J) were randomly assigned into Alzheimer's disease transgenic model group (AD group,n=10) and experimental group (n=10) by using random number table method,another 10 C57BL/6J aged normal mice were assigned into elderly group as comparison.The AD group and the experimental group were injected with mNGF to the lateral ventricles of the brain for 3 times (10 days apart),while the elderly group was injected with the same amount of 0.9% sodium chloride injection as comparison.Space exploration experiment was carried out by video tracking analysis system of Morris water maze；evoked population spikes (PS) in hippocampal area CA1 and spontaneous action potentials (AP) were recorded by using whole cell patch clamp；immunohistochemistry was used to detect the expression levels of brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in hippocampal area CA1；Real-time quantitative polymerase chain reaction was used to detect NGF mRNA and BDNF mRNA in the hippocampal area CA1.Results On the 40th day of treatment,the protein-positive expressions of BDNF [(100.51±2.27) ng/mL] and NGF [(159.85±1.23) ng/mL] and the expressions of BDNF mRNA [(72.02±0.98) β-actin] and NGF mRNA [(67.08±1.16) β-actin] in hippocampal area CA1 of brain slices of the experimental group mice increased significantly,and their membrane potential of PS [(63.02±1.25) mV] and AP [(58.57±0.93) mV] decreased with significant differences from those before treatment and the 40th day (all P<0.05).The number of crossing plateau (4.29±0.64) in the experimental group was significantly more than that before treatment and in the AD group (2.85±0.12,2.68±0.24) (F=49.815,232.391,P<0.05).The escape latency in the experimental group [(21.73±0.54) s] was significantly shorter than that in the AD group [(68.59±2.01) s].There were significant differences between the experimental group and AD group and between before and after the treatment in the experimental group (F=2 910.165,3 137.281,P<0.05).The trajectory of the elderly group was mainly located on the original platform,that of the AD group was mainly scattered around,and that of the experimental group was between the two.Conclusions The mice nerve growth factor can promote learning and memory abilities of transgenic model mice with Alzheimer's disease,whose mechanism may be related to the mNGF's nourishment and repairing of nerves by stabilizing membrane potential in hippocampal area CA1,upregulating BDNF and NGF protein and their genetic expressions. |
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