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目的:观察大麻素对背根节神经元ATP诱发的[Ca~(2+)]i升高的影响及机制。方法:培养SD大鼠背根节神经元,采用激光共聚焦技术检测培养神经元[Ca~(2+)]i的变化。结果:ATP(100μmol/L)经P2X受体介导可导致培养的背根节神经元[Ca~(2+)]i增高(P<0.05);大麻素受体激动剂CP55940预孵育10 min可剂量依赖性地抑制背根节神经元ATP所致的[Ca~(2+)]i升高(P<0.05);CB1受体(cannabinoid receptor 1,B1R)的拮抗剂AM251(10μmol/L)、CB2受体(Cannabinoid receptor 2,CB2R)的拮抗剂AM630(10μmol/L)均可显著降低CP55940(1μmol/L)的抑制效应(P<0.05);腺苷酸环化酶激动剂Forskolin(10μmol/L)可逆转CP55940对ATP的抑制作用(P<0.05)。结论:CP55940可显著抑制背根节神经元ATP诱发的[Ca~(2+)]i升高,CP55940的抑制效应可能是由CB1、CB2受体介导抑制背根节神经元PKA活性所致。
Objective: To observe the effect and mechanism of cannabinoids on ATP-induced elevation of [Ca ~ (2 +)] i in dorsal root ganglion neurons. Methods: Dorsal root ganglion neurons were cultured in SD rats. The changes of [Ca ~ (2 +)] i in cultured neurons were detected by laser scanning confocal microscope. Results: ATP (100μmol / L) could induce the increase of [Ca ~ (2 +)] i in dorsal root ganglion neurons via P2X receptor (P <0.05); preincubation of cannabinoid receptor agonist CP55940 for 10 min ([Ca ~ (2 +]] i increased in dorsal root ganglion neurons (P <0.05) in a dose-dependent manner. Antagonist AM251 (10μmol / L ), And antagonist AM630 (10μmol / L) of CB2 receptor (CB2R) significantly reduced the inhibitory effect of CP55940 (1μmol / L) (P <0.05); adenosine cyclase agonist Forskolin 10μmol / L) reversed the inhibitory effect of CP55940 on ATP (P <0.05). CONCLUSION: CP55940 can significantly inhibit the increase of [Ca ~ (2 +)] i induced by ATP in the dorsal root ganglion neurons. The inhibitory effect of CP55940 may be mediated by the inhibition of the PKA activity of dorsal root ganglion neurons by CB1 and CB2 receptors .