Ashton John C, Smith Paul F, Darlington Cynthia L
Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago Medical School, University of Otago, Dunedin, New Zealand.
Pharmacology. 2008;81(1):18-20. doi: 10.1159/000107663. Epub 2007 Aug 28.
The cannabinoid Delta(9)-tetrahydrocannabinol (Delta(9)-THC) is currently being employed or tested for a number of therapeutic uses. Cannabinoid CB1 receptors are critically involved in adverse memory extinction. It is not known whether an unintended effect of Delta(9)-THC is increased extinction rates of adverse memories. We therefore tested the effect of Delta(9)-THC on adverse memory extinction using an auditory-stimulus/foot shock paradigm. We found that repeated administration of a high dose of Delta(9)-THC over 6 days retarded extinction compared with controls. This is in contrast to other reports and might be a result of endocannabinoid signalling dysfunction due to cannabinoid receptor densensitization.
大麻素Δ⁹-四氢大麻酚(Δ⁹-THC)目前正被用于多种治疗用途或处于测试阶段。大麻素CB1受体在不良记忆消退中起关键作用。目前尚不清楚Δ⁹-THC的一个意外作用是否是增加不良记忆的消退率。因此,我们使用听觉刺激/足部电击范式测试了Δ⁹-THC对不良记忆消退的影响。我们发现,与对照组相比,连续6天重复给予高剂量的Δ⁹-THC会延迟消退。这与其他报告相反,可能是由于大麻素受体脱敏导致内源性大麻素信号功能障碍的结果。