期刊
PSYCHOPHARMACOLOGY
卷 232, 期 15, 页码 2723-2729出版社
SPRINGER
DOI: 10.1007/s00213-015-3915-0
关键词
Dopamine; Positron emission tomography (PET); Delta 9-Tetrahydrocannabinol (THC); [C-11]raclopride; Striatum; Cannabis
资金
- Rubicon grant from the Netherlands Organisation for Scientific Research
- Medical Research Council [MC_U120097115, 1116129, G0700995] Funding Source: researchfish
- MRC [G0700995, MC_U120097115] Funding Source: UKRI
Elevated dopamine function is thought to play a key role in both the rewarding effects of addictive drugs and the pathophysiology of schizophrenia. Accumulating epidemiological evidence indicates that cannabis use is a risk factor for the development of schizophrenia. However, human neurochemical imaging studies that examined the impact of a dagger 9-tetrahydrocannabinol (THC), the main psychoactive component in cannabis, on striatal dopamine release have provided inconsistent results. The objective of this study is to assess the effect of a THC challenge on human striatal dopamine release in a large sample of healthy participants. We combined human neurochemical imaging data from two previous studies that used [C-11]raclopride positron emission tomography (PET) (n = 7 and n = 13, respectively) to examine the effect of THC on striatal dopamine neurotransmission in humans. PET images were re-analysed to overcome differences in PET data analysis. THC administration induced a significant reduction in [C-11]raclopride binding in the limbic striatum (-3.65 %, from 2.39 +/- 0.26 to 2.30 +/- 0.23, p = 0.023). This is consistent with increased dopamine levels in this region. No significant differences between THC and placebo were found in other striatal subdivisions. In the largest data set of healthy participants so far, we provide evidence for a modest increase in human striatal dopamine transmission after administration of THC compared to other drugs of abuse. This finding suggests limited involvement of the endocannabinoid system in regulating human striatal dopamine release and thereby challenges the hypothesis that an increase in striatal dopamine levels after cannabis use is the primary biological mechanism underlying the associated higher risk of schizophrenia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据