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首页> 外文期刊>Life sciences >EVALUATION OF CAMP INVOLVEMENT IN CANNABINOID-INDUCED ANTINOCICEPTION
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EVALUATION OF CAMP INVOLVEMENT IN CANNABINOID-INDUCED ANTINOCICEPTION

机译：大麻诱导的止痛药中营地参与度的评估

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It has been proposed that cannabinoids act at a Gi protein-coupled receptor to produce antinociception. One action of Gi-proteins is to decrease intracellular cAMP via inhibition of adenylyl cyclase activity. Although cannabinoid inhibition of forskolin-stimulated adenylyl cyclase is used as a confirmation of functional cannabinoid receptors, it is unknown whether this second messenger system specifically mediates cannabinoid-induced antinociception. This in vivo study was conducted using enantiomeric cAMP analogs, Rp-cAMPS (an antagonist) and Sp-cAMPS (an agonist), and the cAMP agonist Cl-cAMP to test the hypothesis that cannabinoid-induced antinociception is due to decreased adenylyl cyclase activity. None of the cAMP analogs, forskolin, or 1,9-dideoxy-forskolin affected Delta(9)-THC or CP-55,940-induced antinociception produced by intrathecal (i.t.) or intracerebroventricular (i.c.v.) injections in mice. Experiments were also conducted to investigate whether i.c.v. administration of Sp-cAMPS would block i.c.v. cannabinoid-induced antinociception in rats. Sp-cAMPS failed to block CP-55,940-induced antinociception. However, Sp-cAMPS produced hyper-excitability and reactive behavior indicating that it did elicit a pharmacological effect. Although, adenylyl cyclase may mediate other cannabinoid-induced actions, these results do antinociception. Alternatively, other effector systems such as calcium or potassium channels coupled to cannabinoid receptors may mediate cannabinoid-induced antinociception. [References: 28]
机译：已经提出，大麻素作用于Gi蛋白偶联受体以产生抗伤害感受。 Gi蛋白的一种作用是通过抑制腺苷酸环化酶活性来降低细胞内的cAMP。尽管使用大麻素抑制福司可林刺激的腺苷酸环化酶来确认功能性大麻素受体，但尚不清楚第二种信使系统是否特异性介导大麻素诱导的抗伤害感受。这项体内研究是使用对映体cAMP类似物，Rp-cAMPS（拮抗剂）和Sp-cAMPS（激动剂）和cAMP激动剂Cl-cAMP进行的，以测试大麻素诱导的抗伤害感受是由于腺苷酸环化酶活性降低引起的假说。由小鼠鞘内（i.t.）或脑室内（i.c.v.）注射产生的cAMP类似物，福司高林或1,9-二脱氧-福司高林均不会影响Delta（9）-THC或CP-55,940诱导的镇痛作用。还进行了实验，以调查是否Sp-cAMPS的管理会阻止i.c.v.大麻素诱导的大鼠抗伤害感受。 Sp-cAMPS无法阻止CP-55,940诱导的抗伤害感受。但是，Sp-cAMPS产生了超兴奋性和反应性，表明确实引起了药理作用。尽管腺苷酸环化酶可能介导其他大麻素诱导的作用，但这些结果确实具有抗伤害作用。或者，其他效应系统，例如与大麻素受体偶联的钙或钾通道，可以介导大麻素诱导的抗伤害感受。 [参考：28]

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