中缝背核微量注射L-N-硝基精氨酸甲酯抑制大鼠乙状结肠痛

用Fos免疫组织化学、烟酰胺腺嘌呤二核苷酸磷酸黄递酶(nicotinamide adenine dinucleotide phosphate—di—aphorase,NADPH-d)组织化学及微量注射技术,观察大鼠乙状结肠注射甲醛(5％)诱发的大鼠乙状结肠炎性痛过程中中缝背核一氧化氮合酶(nitric oxide synthase,NOS)神经元的变化,同时观察中缝背核微量注射L-N-硝基精氨酸甲酯(LNAME)对乙状结肠痛的调控作用。结果表明,(1)乙状结肠注射甲醛后,大鼠出现明显的内脏痛反应,中缝背核NOS神经元表达明显增多,中缝背核内出现大量Fos蛋白,在整个中缝背核内均有分布,并且出现Fos／NOS双标神经元,约占中缝背核NOS神经元总数的8％,与生理盐水对照组相比差异有显著性;(2)中缝背核注射L-NAME后,可以明显减少乙状结肠炎性痛大鼠的疼痛学评分及脊髓相应节段Fos蛋白。上述结果提示,中缝背核NOS神经元参与调控大鼠乙状结肠痛,NO在中缝背核促进内脏伤害性信息的传递。

Microinjection of L-NAME into dorsal raphe nucleus inhibits nociceptive response in sigmoid pain model of rats

By means of Fos immunocytochemistry, nicotinamide adenine dinucleotide phosphate - dia-phorase (NADPH-d) histochemistry and microinjection methods, the role of nitric oxide synthase (NOS) ofdorsal raphe (DR) neurons in the modulation of rats sigmoid pain was studied. The results showed: (1 )Rats exhibited aversive behavioral responses related to visceral pain after injecting formalin into the sigmoidwall. NOS neurons in DR were up-regulated, in addition, about 8% of NOS-labeled neurons were Fos posi-tive. By contrast, there was no Fos/NOS double-labeled neurons in the control group. (2) Formalin-in-duced sigmoid pain scores and the expression of Fos in the spinal cord at S1 segment were decreased aftermicroinjecting L-NAME into the DR. These findings suggest that NOS neurons are involved in the modula-tion of formalin-induced sigmoid pain and that NO may play an important role in the transmission of visceralnociceptive message in the midbrain.