Piomelli Daniele
Department of Pharmacology, University of California, Irvine, Irvine, CA 92697-4625, USA.
Neuropharmacology. 2004;47 Suppl 1:359-67. doi: 10.1016/j.neuropharm.2004.07.018.
The active principle of marijuana, Delta9-tetrahydrocannabinol (Delta9-THC), exerts its pharmacological effects by binding to selective receptors present on the membranes of neurons and other cells. These cannabinoid receptors are normally engaged by a family of lipid mediators, called endocannabinoids, which are thought to participate in the regulation of a diversity of brain functions, including pain, mood, appetite and memory. Marijuana use may lead to adaptive changes in endocannabinoid signaling, and these changes might contribute to effects of marijuana as well as to the establishment of marijuana dependence. In the present article, I outline current views on how endocannabinoid substances are produced, released, and deactivated in the brain. In addition, I review recent progress on the development of pharmacological agents that interfere with endocannabinoid deactivation and discuss their potential utility in the treatment of marijuana dependence and other aspects of drug abuse.
大麻的活性成分Δ9-四氢大麻酚（Δ9-THC），通过与神经元和其他细胞膜上存在的选择性受体结合发挥其药理作用。这些大麻素受体通常由一类脂质介质（称为内源性大麻素）激活，内源性大麻素被认为参与多种脑功能的调节，包括疼痛、情绪、食欲和记忆。使用大麻可能导致内源性大麻素信号传导的适应性变化，这些变化可能促成大麻的作用以及大麻依赖的形成。在本文中，我概述了目前关于内源性大麻素物质在大脑中如何产生、释放和失活的观点。此外，我回顾了干扰内源性大麻素失活的药理制剂开发的最新进展，并讨论了它们在治疗大麻依赖和药物滥用其他方面的潜在用途。
