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首页> 外文期刊>Arthritis & Rheumatism >Tonic modulation of spinal hyperexcitability by the endocannabinoid receptor system in a rat model of osteoarthritis pain †
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Tonic modulation of spinal hyperexcitability by the endocannabinoid receptor system in a rat model of osteoarthritis pain †

机译：内源性大麻素受体系统在骨关节炎疼痛大鼠模型中对脊髓兴奋性的强直调节作用†

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ObjectiveTo investigate the impact of an experimental model of osteoarthritis (OA) on spinal nociceptive processing and the role of the inhibitory endocannabinoid system in regulating sensory processing at the spinal level.MethodsExperimental OA was induced in rats by intraarticular injection of sodium mono-iodoacetate (MIA), and the development of pain behavior was assessed. Extracellular single-unit recordings of wide dynamic range (WDR) neurons in the dorsal horn were obtained in MIA-treated rats and saline-treated rats. The levels of endocannabinoids and the protein and messenger RNA levels of the main synthetic enzymes for the endocannabinoids (N-acyl phosphatidylethanolamine phospholipase D [NAPE-PLD] and diacylglycerol lipase [DAGL]) in the spinal cord were measured.ResultsLow-weight (10 gm) mechanically evoked responses of WDR neurons were significantly (P 0.05) facilitated 28 days after MIA injection compared with the responses in saline-treated rats, and spinal cord levels of anandamide and 2-arachidonoyl glycerol (2-AG) were increased in MIA-treated rats. Protein levels of NAPE-PLD and DAGL, which synthesize anandamide and 2-AG, respectively, were elevated in the spinal cords of MIA-treated rats. The functional role of endocannabinoids in the spinal cords of MIA-treated rats was increased via activation of cannabinoid 1 (CB1) and CB2 receptors, and blockade of the catabolism of anandamide had significantly greater inhibitory effects in MIA-treated rats compared with control rats.ConclusionOur findings provide new evidence for altered spinal nociceptive processing indicative of central sensitization and for adaptive changes in the spinal cord endocannabinoid system in an experimental model of OA. The novel control of spinal cord neuronal responses by spinal cord CB2 receptors suggests that this receptor system may be an important target for the modulation of pain in OA.
机译：目的研究骨关节炎（OA）实验模型对脊髓伤害感受性加工的影响以及抑制性内源性大麻素系统在脊髓水平上调节感觉加工的作用。方法通过关节腔内注射单碘乙酸钠（MIA）诱导大鼠实验性OA ），并评估疼痛行为的发展。在MIA治疗的大鼠和生理盐水治疗的大鼠中，获得了背角中宽动态范围（WDR）神经元的细胞外单细胞记录。测量了脊髓中内源性大麻素的水平以及内源性大麻素的主要合成酶（N-酰基磷脂酰乙醇胺磷脂酶D [NAPE-PLD]和二酰基甘油脂酶[DAGL]）的蛋白质和信使RNA的水平。结果低体重（10） gm）与注射盐水的大鼠相比，MIA注射后28天，WDR神经元的机械诱发反应显着（P <0.05）促进，脊髓中anandamide和2-arachidonoyl glycerol（2-AG）的水平增加。经MIA处理的大鼠。在MIA处理的大鼠的脊髓中，分别合成anandamide和2-AG的NAPE-PLD和DAGL的蛋白质水平升高。通过激活大麻素1（CB 1 ）和CB 2 受体的激活以及对MIA分解代谢的阻断，增强了MIA处理的大鼠脊髓中内源性大麻素的功能。与对照组相比，anandamide在MIA治疗的大鼠中具有明显更大的抑制作用。结论我们的发现为OA实验模型中指示中枢敏化作用的脊髓伤害性加工改变和脊髓内源性大麻素系统的适应性变化提供了新的证据。脊髓CB 2 受体对脊髓神经元反应的新颖控制表明该受体系统可能是OA疼痛调节的重要靶标。

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