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本研究通过鞘内注射 c-fos反义寡聚脱氧核苷酸 (antisense oligodeoxynucleotide,AS-ODN)封闭背角中 F os蛋白的表达 ,观察了 Fos蛋白合成和慢痛反应的关系 ,并分析 Fos蛋白合成和强啡肽 A(Dyn A)表达之间的关系。实验组动物 (n=5 )鞘内预先注射 c-fos的 AS-ODN(5 0μg,5μl) ,另两个对照组 (每组 n=5 )分别注射等量生理盐水和 AS-ODN的反序核苷酸 (reverseoligodeoxynucleotides,RS-ODN,5 0μg,5μl) ;4h后 ,各组动物均在一侧后肢脚掌皮下注射 formalin(5 % ,5 0μl) ,并立即用计算动物舔拭注射侧后脚掌累计时间的方法 ,检测大鼠的伤害性行为反应 ,行为检测后 1h处死动物 ,用免疫组化方法检查脊髓背角中 Fos蛋白阳性神经元的数量和强啡肽 A(1～ 8)的表达量。结果发现 ,和两个对照组相比 ,实验组动物 Formalin诱发的伤害性行为反应的第二相明显减弱 ,同时 Form alin注射侧背角 F os蛋白样免疫阳性细胞的数量和 Dyn A含量的灰度值明显减少。本研究结果提示 ,外周伤害性刺激引起的长期持续的痛反应是以 c-fos基因表达增加及受其调控的 Dyn A表达上调为基础的 ,由此推测在脊髓背角神经元中 Fos蛋白和 Dyn A表达的增强可能是出现慢性痛行为反应和痛过敏状态的基础
In this study, the F os protein expression in closed dorsal horn was detected by intrathecal injection of antisense oligodeoxynucleotide (AS-ODN), the relationship between Fos protein synthesis and slow pain reaction was observed, and Fos Relationship between protein synthesis and dynorphin A (Dyn A) expression. AS-ODN (50 μg, 5 μl) of intrathecal c-fos was injected into the experimental group (n = 5), and the other two control groups (n = 5 each) After 4h, formalin (5%, 50μl) was subcutaneously injected into the paws of the hindlimbs of each group, and animals were immediately licked on the injected side with RSV ODN (50μg, 5μl) The rats were sacrificed at 1 hour after behavioral testing. The number of Fos protein positive neurons in spinal dorsal horn and the expression of dynorphin A (1 ~ 8) were detected by immunohistochemistry The amount of expression. The results showed that compared with the two control groups, the second phase of the nociceptive behavior induced by Formalin in the experimental group was significantly weakened, while the number of F os protein-like immunoreactive cells and Dyn A content in the dorsal horn of Form alin injected Degree significantly reduced. Our results suggest that chronic long-term pain induced by peripheral noxious stimulation is based on an increase in c-fos gene expression and up-regulation of Dyn A expression, suggesting that Fos protein and The increased expression of Dyn A may be the basis for the appearance of chronic pain behavior reactions and hyperalgesia