损毁炎症大鼠下丘脑弓状核对痛觉过敏的影响

摘要

目的 观察损毁炎症大鼠下丘脑弓状核( ARC)对炎症大鼠痛觉过敏的影响.方法 用完全弗氏佐剂(CFA)建立大鼠外周组织炎症模型；采用新生期大鼠注射谷氨酸单钠(MSG)破坏ARC神经元或电解损毁成年大鼠的ARC；用辐射热-缩腿法测定炎症大鼠热痛阈的变化,用von Frey法测定机械痛阈的变化.结果 (1)大鼠在注射CFA后热痛阈和机械痛阈均明显降低,出现痛觉过敏,3h达到高峰,到第3天有所恢复并且稳定维持痛觉过敏状态,一直维持到本实验观察的第14天；(2)新生期注射MSG的大鼠在注射CFA后3h,热痛阈和机械痛阈也明显降低,出现痛觉过敏,但其痛阈降低的幅度明显小于注射高渗盐水对照的CFA组；(3)CFA炎症大鼠在电解损毁ARC之后,其热痛阈和机械痛阈与假损毁组相比,均明显上升,即痛觉过敏减轻.结论 在外周存在炎症条件下,两种方法损毁ARC都能减轻痛觉过敏.提示ARC参与外周组织炎症引起的痛觉过敏,对痛觉过敏的发生有下行易化作用.%Objective To study the effect of hypothalamic arcuate nucleus ( ARC) lesion on the hyperalgesia of inflammatory rats and investigate the descending modulation on hyperalgesia from ARC. Methods The peripheral inflammation model was established by sub-plantar injection of complete Freund' s adjuvant ( CFA) in rats. ARC was lesioned electrolytically and by neonatal injection of monosodium glutamate ( MSG). The thermal pain threshold was measured by radiant heat-withdrawal method and the mechanical pain threshold was measured by von Frey method. Results ( 1 ) Hyperalgesia ( decrease of thermal and mechanical pain threshold) appeared after injection of CFA, the peak time was at 3h, and the hyperalgesic state could last for 14 days (2) In MSG-treated neonatal rats the thermal and mechanical pain threshold were decreased at 3h after CFA injection, but the amplitude of decrement was significantly less as compared with that in the control hyperosmotic saline-treated rats. Results indicated that the CFA-produced hyperalgesia was significantly attenuated after the neuronalrndamage of ARC induced by MSG neonatally. (3) In CFA-induced inflammatory rats both thermal and mechanical pain thresholds were increased significantly after electrolytical lesion of ARC as compared with those in the sham lesioned rats, showing that ARC lesion could also attenuate the hyperalgesia induced by CFA. Conclusion Under the condition of peripheral inflammation, both neonatal MSG injection and electrolytical ARC lesion could attenuate the hyperalgesia. It suggests that ARC takes part and presumably mediates its descending facilitatory control on the hyperalgesia induced by peripheral tissue inflammation.