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Spinal cord dynorphin may modulate nociception via a kappa-opioid receptor in chronic arthritic rats.

作者信息

Millan M J, Millan M H, Pilcher C W, Członkowski A, Herz A, Colpaert F C

出版信息

Brain Res. 1985 Aug 5;340(1):156-9. doi: 10.1016/0006-8993(85)90786-3.

DOI:10.1016/0006-8993(85)90786-3
PMID:2862957
Abstract

Inoculation of rats with Mycobacterium butyricum produced an arthritis of the limbs which revealed an enhanced sensitivity to noxious mechanical pressure (hyperalgesia). Arthritic rats displayed a pronounced rise in immunoreactive dynorphin in lumbo-sacral spinal cord which correlated both with the intensity and time-course of this hyperalgesia. MR-2266, a relatively preferential antagonist at the chi-opioid receptor (at which dynorphin is considered to act) potentiated this hyperalgesia. In contrast, MR 2267 (its inactive stereo-isomer) was ineffective. Further, naloxone (a weak chi-antagonist), and ICI 154,129 (a preferential delta-antagonist) were, in each case, inactive. The data demonstrate a pronounced response of spinal dynorphin to chronic arthritic pain in the rat. In addition, they raise the possibility of a function of spinal DYN, via a chi-receptor, in the modulation of chronic arthritic pain.

摘要

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