Verty Aaron N A, McGregor Iain S, Mallet Paul E
School of Psychology, University of New England, Armidale, NSW 2351, Australia.
Brain Res. 2004 Sep 10;1020(1-2):188-95. doi: 10.1016/j.brainres.2004.06.033.
A large body of evidence supports the notion that Delta9-tetrahydrocannabinol (THC) stimulates food intake by its actions on CB1 cannabinoid receptors. Indirect evidence also suggests a role for dopamine (DA) receptors in mediating THC-induced feeding. In the present study, a series of experiments involving intraperitoneal drug administration in rats were conducted to further investigate the interaction between cannabinoid and dopamine receptors in feeding behaviour. Male Wistar rats were habituated to the test environment and injection procedure, and then were injected with vehicle alone, the dopamine D1-like receptor antagonist SCH 23390 (0.005, 0.01, 0.5 or 0.1 mg/kg), THC (0.1, 0.5 or 1.0 mg/kg) or SCH 23390 and THC combined. Food intake and locomotor activity were then measured for 120 min. Results revealed that administration of SCH 23390 dose-dependently decreased food intake while THC dose-dependently increased feeding. Furthermore, SCH 23390 attenuated feeding induced by THC at a dose that did not affect feeding on its own. These findings provide direct evidence for the existence of cannabinoid-dopamine interactions in feeding behaviour and suggest that dopamine D1 signalling is necessary for cannabinoids to stimulate food intake.
大量证据支持这样一种观点，即Δ9-四氢大麻酚（THC）通过作用于CB1大麻素受体来刺激食物摄入。间接证据还表明多巴胺（DA）受体在介导THC诱导的进食中发挥作用。在本研究中，进行了一系列在大鼠腹腔内给药的实验，以进一步研究大麻素受体与多巴胺受体在进食行为中的相互作用。雄性Wistar大鼠适应测试环境和注射程序，然后分别注射溶剂、多巴胺D1样受体拮抗剂SCH 23390（0.005、0.01、0.5或0.1mg/kg）、THC（0.1、0.5或1.0mg/kg）或SCH 23390与THC的组合。随后测量120分钟内的食物摄入量和运动活动。结果显示，给予SCH 23390可剂量依赖性地减少食物摄入量，而给予THC则可剂量依赖性地增加进食量。此外，SCH 23390以不影响自身进食的剂量减弱了THC诱导的进食。这些发现为进食行为中存在大麻素-多巴胺相互作用提供了直接证据，并表明多巴胺D1信号传导是大麻素刺激食物摄入所必需的。
