Zhang Ji, Hoffert Cyrla, Vu Huy Khang, Groblewski Thierry, Ahmad Sultan, O'Donnell Dajan
AstraZeneca R&D, Montréal, 7171, Frederick-Banting, Ville St-Laurent, Quebec, H4S 1Z9, Canada.
Eur J Neurosci. 2003 Jun;17(12):2750-4. doi: 10.1046/j.1460-9568.2003.02704.x.
Cannabinoids have been considered for some time as potent therapeutic agents in chronic pain management. Central and systemic administration of natural, synthetic and endogenous cannabinoids produce antinociceptive and antihyperalgesic effects in both acute and chronic animal pain models. Although much of the existing data suggest that the analgesic effects of cannabinoids are mediated via neuronal CB1 receptors, there is increasing evidence to support a role for peripheral CB2 receptors, which are expressed preferentially on immune cells. As yet, little is known about the central contribution of CB2 in neuropathic pain states. We report here that chronic pain models associated with peripheral nerve injury, but not peripheral inflammation, induce CB2 receptor expression in a highly restricted and specific manner within the lumbar spinal cord. Moreover, the appearance of CB2 expression coincides with the appearance of activated microglia.
一段时间以来，大麻素一直被视为慢性疼痛管理中的有效治疗剂。在急性和慢性动物疼痛模型中，天然、合成和内源性大麻素的中枢和全身给药均产生抗伤害感受和抗痛觉过敏作用。尽管现有许多数据表明大麻素的镇痛作用是通过神经元CB1受体介导的，但越来越多的证据支持外周CB2受体的作用，CB2受体优先在免疫细胞上表达。迄今为止，关于CB2在神经性疼痛状态中的中枢作用知之甚少。我们在此报告，与外周神经损伤相关而非外周炎症相关的慢性疼痛模型，在腰脊髓内以高度受限和特异的方式诱导CB2受体表达。此外，CB2表达的出现与活化小胶质细胞的出现相吻合。
