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首页> 外文期刊>Progress in Natural Science: Communication of State Key Laboratories of China >Anti-nociceptive role of neuropeptide Y in the nucleus accumbens in rats with inflammation, an effect modulated by mu- and kappa-opioid receptors
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Anti-nociceptive role of neuropeptide Y in the nucleus accumbens in rats with inflammation, an effect modulated by mu- and kappa-opioid receptors

机译:神经肽Y在炎症大鼠伏伏核中的抗伤害感受作用,这种作用由mu和kappa类阿片受体调节

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Recent study in our laboratory showed that neuropeptide Y (NPY) plays an antinociceptive role in the nucleus accumbens (NAc) in intact rats. The present study was performed to further investigate the effect of NPY in nociceptive modulation in the NAc of rats with inflammation, and the possible interaction between NPY and the opioid systems. Experimental inflammation was induced by subcutaneous injection of carrageenan into the left hindpaw of rats. Intra-NAc administration of NPY induced a dose-dependent increase of hindpaw withdrawal latencies (HWLs) to thermal and mechanical stimulations in rats with inflammation. The anti-nociceptive effect of NPY was significantly blocked by subsequent intra-NAc injection of the Y1 receptor antagonist NPY28-36, suggesting an involvement of Y1 receptor in the NPY-induced anti-nociception. Furthermore, intra-NAc administration of the opioid antagonist naloxone significantly antagonized the increased HWLs induced by preceding intra-NAc injection of NPY, suggesting an involvement of the endogenous opioid system in the NPY-induced anti-nociception in the NAc during inflammation. Moreover, the NPY-induced anti-nociception was attenuated by following intra-NAc injection of the μ-opioid antagonist β-funaltrexamine (β-FNA), and κ-opioid antagonist nor-binaltorphimine (nor-BNI), but not by δ-opioid antagonist naltrindole, indicating that μ- and κ-opioid receptors, not δ-opioid receptor, are involved in the NPY-induced anti-nociception in the NAc in rats with inflammation.
机译:我们实验室的最新研究表明,神经肽Y(NPY)在完整大鼠的伏伏核(NAc)中起镇痛作用。进行本研究以进一步研究NPY在炎症大鼠NAc中对伤害性调节中的作用以及NPY与阿片类药物系统之间可能的相互作用。通过将角叉菜胶皮下注射到大鼠的左后爪中诱发实验性炎症。 NPY的NAc内给药对炎症大鼠的热刺激和机械刺激引起后爪退缩潜伏期(HWL)的剂量依赖性增加。随后的NAc内Y1受体拮抗剂NPY28-36的NAc注射显着阻断了NPY的抗伤害感受作用,表明Y1受体参与了NPY诱导的抗伤害感受。此外,阿片类药物拮抗剂纳洛酮的NAC内给药显着拮抗了先前NAC内注射NPY诱导的HWL升高,这表明内源性阿片样物质系统参与了炎症过程中NPY诱导的NAC的抗伤害感受。此外,在NAc内注射μ阿片类拮抗剂β-富纳曲胺(β-FNA)和κ阿片类拮抗剂去甲双萘酚(nor-BNI)后,NPY诱导的抗伤害感受减弱,但δ却没有-阿片拮抗剂纳曲酮,表明μ和κ阿片受体而不是δ阿片受体参与了炎症大鼠NAc中NPY诱导的抗伤害感受。

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