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目的 :在背根节 (DRG)慢性压迫模型上 ,采用单纤维记录神经元自发放电和生化检测受损组织中蛋白激酶A(proteinkinase ,PKA)活性的方法 ,研究PKA在DRG压迫损伤后感觉神经元中自发放电的作用。结果 :压迫损伤侧DRG组织中的PKA磷酸化PepTag肽百分数为 2 5 .5 1± 2 .6 2 % ,较未受压迫侧和正常组DRG组织明显增加 (P <0 .0 5 )。PKA催化亚单位抑制剂H 89(1 0 μM )可以明显抑制受损DRG神经元的自发放电 ,抑制百分数为 76 .91± 1 3.79%。结论 :受损DRG组织中PKA活性上调 ,高活性的PKA参与介导受损DRG神经元的自发放电。
OBJECTIVE: To investigate the effect of PKA on the expression of PKA in DRG-induced chronic neuropathic pain (DRG) models using spontaneous electrical discharge and biochemical detection of single neurofibrillary neurons. Yuan spontaneous discharge role. Results: The percentage of PKA phosphorylated PepTag peptide in injured DRG tissues was 25.51 ± 2.62%, which was significantly higher than that in uncompressed and normal DRG tissues (P <0.05). PKA catalytic subunit inhibitor H 89 (10 μM) significantly inhibited the spontaneous discharge of injured DRG neurons with a percentage inhibition of 76.91 ± 1 3.79%. CONCLUSION: PKA activity is up-regulated in injured DRG tissues and highly active PKA is involved in mediating spontaneous firing of impaired DRG neurons.