School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, 264005, P.R. China.
Neurobiology Laboratory, College of Life Sciences, Peking University, Beijing, 100871, P.R. China.
Sci Rep. 2017 Nov 10;7(1):15317. doi: 10.1038/s41598-017-13944-6.
The present study was performed to explore the role of galanin and galanin receptor 1 (GalR 1) in nociceptive modulation in the central nucleus of amygdala (CeA) in normal rats and rats with neuropathy, and the involvement of GalR 1 and PKC was also investigated. The hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations were increased in a dose-dependent manner after intra-CeA injection of galanin in both normal rats and rats with neuropathy. The increased HWLs were significantly attenuated by intra-CeA injection of galanin receptor antagonist M40, indicating an involvement of galanin receptor in nociceptive modulation in CeA. Furthermore, intra-CeA administration of the GalR 1 agonist M 617 induced increases in HWLs in normal rats, suggesting that GalR 1 may be involved in galanin-induce antinociception in CeA. Additionally, intra-CeA injection of the PKC inhibitor inhibited galanin-induced antinociception, showing an involvement of PKC in galanin-induced antinociception in CeA of normal rats. Moreover, there was a significant increase in GalR1 content in CeA in rats with neuropathy than that in normal rats. These results illustrated that galanin induced antinociception in CeA in normal rats and rats with neuropathy, and there is an up-regulation of GalR1 expression in rats with neuropathy.
本研究旨在探讨甘丙肽和甘丙肽受体 1(GalR1)在正常大鼠和神经病变大鼠杏仁中央核(CeA)中痛觉调制中的作用,并探讨 GalR1 和 PKC 的参与情况。在正常大鼠和神经病变大鼠中,侧脑室注射甘丙肽后,热和机械刺激的后爪退缩潜伏期(HWL)呈剂量依赖性增加。侧脑室注射甘丙肽受体拮抗剂 M40 可显著减弱增加的 HWL,表明甘丙肽受体参与 CeA 中的痛觉调制。此外,侧脑室给予 GalR1 激动剂 M617 可增加正常大鼠的 HWL,表明 GalR1 可能参与 CeA 中甘丙肽诱导的抗伤害感受。此外,PKC 抑制剂的侧脑室注射抑制了甘丙肽诱导的抗伤害感受,表明 PKC 参与了正常大鼠 CeA 中甘丙肽诱导的抗伤害感受。此外,神经病变大鼠 CeA 中的 GalR1 含量明显高于正常大鼠。这些结果表明,甘丙肽在正常大鼠和神经病变大鼠的 CeA 中诱导抗伤害感受,并且神经病变大鼠中 GalR1 的表达上调。