Jia Y, Linden D R, Serie J R, Seybold V S
Department of Cell Biology and Neuroanatomy, University of Minnesota, Minneapolis 55455, USA.
Neurosci Lett. 1998 Jun 26;250(1):21-4. doi: 10.1016/s0304-3940(98)00430-3.
Regulation of nociceptin/orphanin FQ neurotransmission in conjunction with peripheral inflammation and hyperalgesia was explored, using receptor autoradiography. Binding of [3H]nociceptin was quantified in spinal segment L4 of rats at 2, 4 and 8 days following injection of complete Freund's adjuvant (CFA) into one hind-paw. Densitometric analysis of autoradiograms showed that [3H]nociceptin binding increased in medial and lateral laminae I-II bilaterally 4 days following injection of CFA compared to untreated rats; no change in binding occurred in lamina X at the times examined. Biochemical studies confirmed that the specific binding of [3H]nociceptin to sections of rat brain was consistent with the binding characteristics of the nociceptin receptor. These results suggest that spinal nociceptin receptors are upregulated during hyperalgesia. This response may enhance endogenous mechanisms of antinociception to attenuate the hyperalgesia induced by CFA.
采用受体放射自显影技术，研究了伤害感受素/孤啡肽FQ神经传递与外周炎症和痛觉过敏的关系。在大鼠一侧后爪注射完全弗氏佐剂（CFA）后2天、4天和8天，对L4脊髓节段中[3H]伤害感受素的结合进行定量分析。放射自显影片的密度分析显示，与未处理的大鼠相比，注射CFA后4天，双侧I-II层内侧和外侧的[3H]伤害感受素结合增加；在所检查的时间点，X层的结合没有变化。生化研究证实，[3H]伤害感受素与大鼠脑切片的特异性结合与伤害感受素受体的结合特性一致。这些结果表明，在痛觉过敏期间，脊髓伤害感受素受体上调。这种反应可能会增强内源性抗伤害感受机制，以减轻CFA诱导的痛觉过敏。
