κ阿片受体拮抗剂和N-甲基-D-天冬氨酸受体拮抗剂影响强啡肽诱导的脊髓电生理损伤。

Kappa opioid receptor antagonist and N-methyl-D-aspartate receptor antagonist affect dynorphin-induced spinal cord electrophysiologic impairment.

作者信息

Chen Yu, Xiang Liangbi, Liu Jun, Zhou Dapeng, Yu Hailong, Wang Qi, Han Wenfeng, Ren Weijian

机构信息

Department of Orthopedics, General Hospital of Shenyang Military Area Command of Chinese PLA, Shenyang 110016, Liaoning Province, China.

出版信息

Neural Regen Res. 2012 Mar 5;7(7):523-7. doi: 10.3969/j.issn.1673-5374.2012.07.008.

DOI:10.3969/j.issn.1673-5374.2012.07.008

PMID:25745439

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4348999/

Abstract

The latencies of motor- and somatosensory-evoked potentials were prolonged to different degrees, and wave amplitude was obviously decreased, after injection of dynorphin into the rat subarachnoid cavity. The wave amplitude and latencies of motor- and somatosensory-evoked potentials were significantly recovered at 7 and 14 days after combined injection of dynorphin and either the kappa opioid receptor antagonist nor-binaltorphimine or the N-methyl-D-aspartate receptor antagonist MK-801. The wave amplitude and latency were similar in rats after combined injection of dynorphin and nor-binaltorphimine or MK-801. These results suggest that intrathecal injection of dynorphin causes damage to spinal cord function. Prevention of N-methyl-D-aspartate receptor or kappa receptor activation lessened the injury to spinal cord function induced by dynorphin.

摘要

向大鼠蛛网膜下腔注射强啡肽后，运动诱发电位和躯体感觉诱发电位的潜伏期不同程度延长，波幅明显降低。在联合注射强啡肽与κ阿片受体拮抗剂nor - 纳洛酮啡或N - 甲基 - D - 天冬氨酸受体拮抗剂MK - 801后7天和14天，运动诱发电位和躯体感觉诱发电位的波幅和潜伏期显著恢复。联合注射强啡肽与nor - 纳洛酮啡或MK - 801的大鼠的波幅和潜伏期相似。这些结果表明，鞘内注射强啡肽会损害脊髓功能。预防N - 甲基 - D - 天冬氨酸受体或κ受体激活可减轻强啡肽诱导的脊髓功能损伤。