孤啡肽受体 2 的激活在神经病理性疼痛大鼠伏隔核中发挥抗伤害作用。
The activation of galanin receptor 2 plays an antinociceptive effect in nucleus accumbens of rats with neuropathic pain.
机构信息
Department of Physiology, School of Basic Medicine, Kunming Medical University, Kunming, 650500, Yunnan, China.
Department of Oncology, Affiliated Hospital, Yunnan University, Kunming, Yunnan, China.
出版信息
J Physiol Sci. 2021 Feb 5;71(1):6. doi: 10.1186/s12576-021-00790-5.
Our previous research has shown that galanin plays an antinociceptive effect via binding to galanin receptors (GalRs) in nucleus accumbens (NAc). This study focused on the involvement of GalR2 in galanin-induced antinociceptive effect in NAc of neuropathic pain rats. The chronic constriction injury of sciatic nerve (CCI) was used to mimic neuropathic pain model. The hind paw withdrawal latency (HWL) to thermal stimulation and hind paw withdrawal threshold (HWT) to mechanical stimulation were measured as the indicators of pain threshold. The results showed that 14 and 28 days after CCI, the expression of GalR2 was up-regulated in bilateral NAc of rats, and intra-NAc injection of GalR2 antagonist M871 reversed galanin-induced increases in HWL and HWT of CCI rats. Furthermore, intra-NAc injection of GalR2 agonist M1145 induced increases in HWL and HWT at day 14 and day 28 after CCI, which could also be reversed by M871. Finally, we found that M1145-induced antinociceptive effect in NAc of CCI rats was stronger than that in intact rats. These results imply that the GalR2 is activated in the NAc from day 14 to day 28 after CCI and GalR2 is involved in the galanin-induced antinociceptive effect in NAc of CCI rats.
我们之前的研究表明，孤啡肽通过与伏隔核（NAc）中的孤啡肽受体（GalR）结合发挥抗伤害作用。本研究旨在探讨 GalR2 在神经病理性疼痛大鼠 NAc 中孤啡肽诱导的抗伤害作用中的作用。坐骨神经慢性缩窄性损伤（CCI）用于模拟神经病理性疼痛模型。热刺激的后爪回缩潜伏期（HWL）和机械刺激的后爪回缩阈值（HWT）作为痛阈的指标进行测量。结果表明，CCI 后 14 天和 28 天，大鼠双侧 NAc 中 GalR2 的表达上调，NAc 内注射 GalR2 拮抗剂 M871 逆转了孤啡肽诱导的 CCI 大鼠 HWL 和 HWT 的增加。此外，CCI 后 14 天和 28 天，NAc 内注射 GalR2 激动剂 M1145 可引起 HWL 和 HWT 的增加，M871 也可逆转这种增加。最后，我们发现 M1145 在 CCI 大鼠 NAc 中的抗伤害作用强于完整大鼠。这些结果表明，CCI 后 14 天至 28 天，NAc 中的 GalR2 被激活，GalR2 参与了 CCI 大鼠 NAc 中孤啡肽诱导的抗伤害作用。
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