Plasma Endocannabinoid Alterations in Individuals with Substance Use Disorder are Dependent on the "Mirror Effect" of Schizophrenia.
Plasma Endocannabinoid Alterations in Individuals with Substance Use Disorder are Dependent on the "Mirror Effect" of Schizophrenia.
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DOI：
10.3389/fpsyt.2012.00085
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发表时间：
2012
影响因子：
4.7
通讯作者：
Potvin S
中科院分区：
文献类型：
--
作者：
Desfossés J;Stip E;Bentaleb LA;Lipp O;Chiasson JP;Furtos A;Venne K;Kouassi E;Potvin S
精神分裂症是一种与物质使用障碍密切相关的复杂精神障碍。从理论上讲，精神分裂症和SUD可能在大脑奖励系统中共享内源性大麻素的改变。主要的内源性大麻素，花生四烯酸和2-花生四烯酸甘油，是结合大麻素受体的脂质。油酰乙醇酰胺（OEA）是一种脂肪酸乙醇酰胺，与过氧化物酶体增殖物激活受体结合。已证明精神分裂症患者的内源性大麻素系统会受损，最近，我们的研究小组发现，患有SUD的精神分裂症患者外周大麻素和OEA水平升高，但在奎硫平治疗3个月后仍未恢复正常。目的比较非精神病物质滥用者和非精神分裂症患者内源性大麻素的水平。方法采用液相色谱-质谱联用技术，检测非精神病性SUD患者、非滥用精神分裂症患者和健康对照者血浆大麻素和OEA水平。以开放标签的方式，所有患者均接受了12周的奎替利治疗。结果物质滥用者中，精神分裂症组的Anandamide和OEA均低于对照组（p < 0.05）。这两种内源性大麻素在非滥用精神分裂症患者中没有变化。奎替利后，大麻素和OEA水平仍显着降低SUD组（p < 0.05）。讨论结合我们以前在双重诊断患者中进行的研究结果，我们的结果表明，根据精神分裂症的存在或不存在，SUD患者外周anandamide和OEA水平以相反的方式受损。内源性大麻素的改变没有改变治疗，这表明他们是性状标记。进一步的研究是必要的，以了解内源性大麻素的作用，滥用药物与精神分裂症和检查治疗的影响。
Schizophrenia is a complex psychiatric disorder strongly associated with substance use disorders. Theoretically, schizophrenia and SUD may share endocannabinoid alterations in the brain reward system. The main endocannabinoids, anandamide, and 2-arachidonoylglycerol, are lipids which bind cannabinoid receptors. Oleoylethanolamide (OEA), a fatty-acid ethanolamide, binds peroxisome proliferator-activated receptors. The endocannabinoid system has been shown to be impaired in schizophrenia, and recently, our group has shown that schizophrenia patients with SUD have elevated peripheral levels of anandamide and OEA that do not normalize after 3-month treatment with quetiapine. Objective For comparative purposes, we aimed to measure endocannabinoids in non-psychosis substance abusers and non-abusing schizophrenia patients. Methods Using liquid chromatography and mass spectrometry, we measured plasma levels of anandamide and OEA in non-psychosis SUD patients, non-abusing schizophrenia patients, and healthy controls. In an open-label manner, all patients received 12-week treatment with quetiapine. Results Anandamide and OEA were reduced in substance abusers without schizophrenia, relative to healthy controls (p < 0.05). Both endocannabinoids were unchanged in non-abusing schizophrenia patients. After quetiapine, anandamide, and OEA levels remained significantly reduced the SUD group (p < 0.05). Discussion Taken together with results of our previous study performed in dual-diagnosis patients, our results suggest that peripheral anandamide and OEA levels are impaired in patients with SUD in opposite ways according to the presence or absence of schizophrenia. Endocannabinoid alterations did not change with treatment, suggesting that they are trait markers. Further studies are necessary to understand the role of endocannabinoids in substance abusers with and without schizophrenia and to examine therapeutic implications.