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目的:观察神经病理性痛条件下细胞外信号调节激酶(extracellular singal-regulated kinase,ERK)对疼痛引起的负性情绪反应的影响。方法:应用Western blot和行为药理学方法,观察腰5脊神经结扎(L5 spinalnerve ligation,SNL)大鼠中央杏仁核外侧囊状部(latero-capsular division of central nucleus of amygdala,CeC)内ERK及磷酸化-ERK(phosphorylated-ERK,p-ERK)的表达情况及ERK磷酸化抑制剂对疼痛引起的负性情绪反应的影响。结果:SNL模型大鼠CeC内p-ERK的表达水平明显升高,与对照组相比,有统计学差异(P<0.05),而总ERK的表达水平则未见组间差异;用超声波检测仪可以检测到SNL大鼠超声发声明显增多,但腹膜腔注射ERK磷酸化的抑制剂U0126后其超声发声被显著抑制。结论:中央杏仁核外侧囊状部内ERK的激活参与了神经病理性痛引起的突触可塑性,在痛相关情绪的产生中发挥了重要作用。
Objective: To observe the effect of extracellular singal-regulated kinase (ERK) on pain-induced negative emotion in patients with neuropathic pain. Methods: Western blot and behavioral pharmacology were used to observe the changes of ERK and phosphorylation in the lateo-capsular division of central nucleus of amygdala (CeC) in lumbar 5 spinal nerve ligated rats (SNL) -ERK (phosphorylated-ERK, p-ERK) expression and ERK phosphorylation inhibitor on pain-induced negative emotional response. Results: The expression of p-ERK in CeC was significantly increased in SNL model rats compared with that in control group (P <0.05), while the expression level of total ERK was no difference between groups. Instrument can detect SNL rats significantly increased sonication, but after intraperitoneal injection of ERK phosphorylation inhibitor U0126 its sonophobia was significantly inhibited. CONCLUSIONS: The activation of ERK in the outer cystic part of the central amygdala participates in synaptic plasticity induced by neuropathic pain and plays an important role in the development of pain-related emotions.