Zachariou V, Goldstein B D
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912-7605, USA.
Brain Res. 1996 Jan 8;706(1):80-8. doi: 10.1016/0006-8993(95)01182-x.
Substance P (SP), a member of the tachykinin peptide family, has been found in high concentrations in the superficial laminae of the dorsal horn and it is thought to play a major role in the transmission of nociceptive information. Dynorphin(1-8), an opioid peptide with high selectivity for the kappa-opioid receptor subtype, is also found in the dorsal horn of the spinal cord. The aim of this study was to determine the effect of dynorphin(1-8) on the release of SP-like-immunoreactivity (SPLI) in the dorsal horn before and during the activation of peripheral nociceptors by a thermal stimulus. A push-pull canula was used to perfuse the dorsal horn of non-anesthetized decerebrate/spinal transected rats and the collected perfusates were assayed for SPLI by using radioimmunoassay. Dynorphin(1-8) applied to the spinal cord at a concentration of 1 microM elicited a 27 +/- 8% decrease in the basal release of SPLI and prevented the increase in the release of SPLI evoked by the application of a noxious thermal stimulus to the ipsilateral hind paw and lower limb. The effect of dynorphin(1-8) was reversed by 2 microM of nor-binaltorphimine (nor-BNI), a selective kappa opioid receptor antagonist. Application of nor-BNI alone to the perfusate resulted in a 62 +/- 23% increase in the basal release of SPLI. In conclusion, dynorphin(1-8) reduces the basal release of SPLI and prevents the increase in the release of SPLI elicited by the application of a noxious cutaneous thermal stimulus. This effect is mediated through the kappa-opioid receptor, which appears to tonically regulate the release of SPLI in the dorsal horn.
P物质(SP)是速激肽肽家族的成员,已发现在背角浅层中浓度很高,并且被认为在伤害性信息传递中起主要作用。强啡肽(1-8)是一种对κ-阿片受体亚型具有高选择性的阿片肽,也存在于脊髓背角中。本研究的目的是确定在热刺激激活外周伤害感受器之前和期间,强啡肽(1-8)对背角中SP样免疫反应性(SPLI)释放的影响。使用推挽式套管灌注未麻醉的去大脑/脊髓横断大鼠的背角,并使用放射免疫测定法对收集的灌流液进行SPLI测定。以1μM的浓度将强啡肽(1-8)应用于脊髓,可使SPLI的基础释放减少27±8%,并阻止因对同侧后爪和下肢施加有害热刺激而引起的SPLI释放增加。2μM的选择性κ阿片受体拮抗剂nor-naltorphimine(nor-BNI)可逆转强啡肽(1-8)的作用。单独将nor-BNI应用于灌流液会导致SPLI的基础释放增加62±23%。总之,强啡肽(1-8)可减少SPLI的基础释放,并阻止因施加有害的皮肤热刺激而引起的SPLI释放增加。这种作用是通过κ-阿片受体介导的,该受体似乎可调节背角中SPLI的释放。