摘要
目的 进一步探讨强啡肽 (Dyn)致脊髓损伤后κ阿片受体机制。 方法 实验分为等渗盐水对照组、DynA(1- 17)致伤组和特异性κ阿片受体拮抗剂nor-BNI治疗组 ,采用 5 -甲基二氢二苯并环庚稀亚氨马来酸 (3H -MK80 1)结合实验测定腹侧脊髓N -甲基 -D -天门冬氨酸(NMDA)受体功能 ,3H -左旋精氨酸 (3H -L -Arg)转化法测定腹侧脊髓原生型和诱导型一氧化氮合酶 (cNOS、iNOS)活性 ,并采用免疫组化技术观测神经元性cNOS(ncNOS)免疫活性。 结果 在蛛网膜下腔注射 2mmol LDynA(1- 17) 10 μl之前 10min ,注射 3mmol Lnor-BNI可显著对抗DynA(1- 17)引起的功能障碍和病理损害 ,并明显对抗DynA(1- 17)引起的3H -MK80 1结合升高及cNOS和iNOS活性增强 ,也明显对抗DynA(1- 17)诱导的脊髓腹角细胞ncNOS免疫活性表达。 结论 Dyn致脊髓损伤过程中 ,κ阿片受体参与Dyn上调腹侧脊髓NMDA受体
Objective [WT5”BZ]To provide new evidences for the κ-opioid receptor mechanism in dynorphin(Dyn)-induced spinal cord injury. Methods The functional activity of N-methyl-D-aspartate (NMDA) receptor and the activity of constitutive and inducible nitric oxide synthase(cNOS and iNOS) were measured respectively with 3 H-MK801 binding and 3 H-L-arginine conversion in the ventral spinal cord of rats after Dyn A(1-17) treatment and selective κ-opioid receptor antagonist nor-BNI pretreatment. Results Pretreatment with nor-BNI (3 mmol/L) 10 min before subarachnoid injection of Dyn A(1-17) (2 mmol/L) could significantly antagonize Dyn-induced permanent paraplegia and increase 3 H-MK801 binding as well as cNOS and iNOS activities in the ventral spinal cord. Nor-BNI also apparently attenuated Dyn-induced increases in immunoreactivities of neuronal cNOS. Conclusions κ-opioid receptor might be involved in the enhancement of the function of NMDA-NOS/NO pathway after Dyn-induced spinal cord injury
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2000年第5期286-288,共3页
Chinese Journal of Trauma
基金
国家自然科学基金资助项目!(39370786)
关键词
强啡肽
脊髓损伤
阿片样受体
一氧化氮
Dynorphin
Spinal cord injury
Receptor, opioid, κ
Excitatory amino acids
Nitric oxide
