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目的 观察福尔马林诱导炎性痛过程中海马蛋白激酶C的表达和神经元形态学变化,并进一步明确海马与疼痛的关系。方法 SD大鼠被随机分为对照组和实验组,实验组又按照注射福尔马林后炎性痛发生时间分为1h, 3h, 12h, 1d, 3d和7d组。应用组织化学和免疫细胞化学方法观察炎性痛过程中海马神经元形态学变化和PKC活性的改变。结果 注射福尔马林1d后海马PKC免疫反应明显上调,PKC被激活并由细胞核转移到膜结构;而“黑神经元”于注射福尔马林后3d最明显,于第7天有所恢复。PKC的活性与神经元的形态学变化均以海马CA3区明显。结论 实验结果表明海马参与了对伤害性信息的调节,而且PKC与炎性痛过程中神经元的损伤有密切关系。
Objective To observe the expression of hippocampal protein kinase C (CIN) and morphological changes of neurons in formalin-induced inflammatory pain, and further clarify the relationship between hippocampus and pain. Methods SD rats were randomly divided into control group and experimental group. The experimental group was also divided into 1h, 3h, 12h, 1d, 3d and 7d groups according to the time of inflammatory pain after injection of formalin. Histological changes and changes of PKC activity in hippocampal neurons during inflammatory pain were observed by histochemical and immunocytochemical methods. RESULTS: After 1 day of formalin injection, the PKC immunoreactivity was significantly up-regulated in the hippocampus, PKC was activated and transferred from the nucleus to the membranous structure, while “black neurons” were the most obvious 3d after formalin injection and recovered on the 7th day . PKC activity and neuronal morphological changes were significantly hippocampal CA3 area. Conclusion The experimental results show that hippocampus participates in the regulation of nociceptive information, and PKC is closely related to the damage of neurons during inflammatory pain.