祁健 陈晨 孟庆溪 赵廷宝.大鼠内侧前额叶皮质内ERK1/2 活化参与脊髓损伤后抑郁情绪[J].,2016,16(31):6015-6018 |
大鼠内侧前额叶皮质内ERK1/2 活化参与脊髓损伤后抑郁情绪 |
Activation of Extracellular Signal-Regulated Kinase1/2 in the MedialPrefrontal Cortex Contributes to Spinal Cord Injury-Induced Depression |
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DOI: |
中文关键词: 细胞外信号调节激酶1/2 内侧前额叶皮质 脊髓损伤 抑郁 |
英文关键词: Extracellular singal-regulated kinase1/2 Medial prefrontal cortex Spinal cord injury Depression |
基金项目:国家自然科学基金项目(31500856);中国博士后科学基金项目(2015M572714);中国博士后特别资助(2016T91010) |
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中文摘要: |
目的:观察细胞外信号调节激酶1/2(ERK1/2)的活化在脊髓损伤引起抑郁中的作用。方法:应用Western blot 和行为药理学
方法,观察脊髓损伤后(SCI)大鼠内侧前额叶皮质内(mPFC)ERK1/2 及磷酸化-ERK1/2(p-ERK1/2)的表达情况及ERK1/2磷酸化抑
制剂U0126 对抑郁样行为的影响。结果:脊髓损伤后的第2 天到第8 周,SCI模型大鼠的BBB 评分均显著低于假手术组,差异具
有统计学意义(p<0.05)。脊髓损伤后8 周-12 周,SCI模型大鼠强迫游泳不动时间与假手术组相比明显缩短,mPFC 内pERK1/2 蛋
白表达水平明显升高,总ERK 1/2 的蛋白水平则未见组间差异,而给予U0126 的大鼠的不动时间与给药之前相比明显延长增加,
mPFC内pERK1/2 蛋白表达水平较SCI模型大鼠明显降低,差异均具有统计学意义(P<0.05)。结论:内侧前额叶皮质内ERK1/2 的
激活参与了脊髓损伤后引起的突触可塑性,在相关的抑郁样行为的产生中发挥了重要的作用。 |
英文摘要: |
Objective:To observe the activation of extracellular singal-regulated kinase1/2 (ERK1/2) on the spinal cord injury-induced
depression.Methods:Western blot and behavioral methods were used to investigate the effect of extracellular signal-regulated kinase1/
2(ERK1/2) activation on the spinal cord injury (SCI) in the medial prefrontal cortex (mPFC), and the effect of inhibiting ERK1/2
phosphorylation by microinjection of U0126 into the mPFC on the depression-like behavior.Results:Fromthe first 2 days to the 8 weeks
after spinal cord injury, the BBB scores of SCI rats was significantly lower than the control group (P<0.05). In 8-12 weeks after spinal
cord injury, the fixed time of forced swimming test in SCI rats was significantly shorter than the control group, the level of pERK1/2 in
the mPFC was upregulated in the SCI rats compared with control rats, not significant difference was found in the total level of ERK 1/2
between different groups, while after U0126 administration, the fixed time was significantly prolonged, the level pERK1/2 in the mPFC
was significantly decreased (P<0.05).Conclusion:The activation of ERK1/2 in the mPFC might contribute to the process of SCI-induced
synaptic plasticity, which played an important role in the depression-like behavior. |
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