Forrester Shawn Y, Jahan Nusrat
Psychiatry, California Institute of Behavioral Neurosciences and Psychology, Fairfield, USA.
Internal Medicine, California Institute of Behavioral Neurosciences and Psychology, Fairfield, USA.
Cureus. 2020 Apr 21;12(4):e7759. doi: 10.7759/cureus.7759.
Escalating cannabis use may be linked to decreased motivation and anhedonia, which are symptoms of depression. Adolescent cannabis users with subthreshold depressive symptoms such as reduced motivation may be susceptible to the development of significant anhedonia in addition to impaired emotional development. The main issue regarding depression within the context of cannabis use is whether or not there is a neurobiological basis linking the two variables. A Medical Subject Headings (MeSH) function PubMed search using the keywords "cannabis, depression, adolescence, endocannabinoid, and temperament" returned 1,109 articles. Data were included from studies that satisfied the following criteria: (i) published within the last 10 years (older studies were included based on relevance), (ii) on adolescent subjects (animal or human), (iii) published in English, (iv) journal articles, systematic reviews, meta-analyses, clinical trials, observational studies (animal or human), (v) on subjects who had unipolar depression with no comorbidities, and (vi) on subjects who used cannabis [with no confounding variables such as the use of ethanol, nicotine, cocaine, lysergic acid diethylamide (LSD), and heroin; and no medical conditions such as comorbid psychosis, mania, or autism]. Depressive symptoms in cannabinoid users were a common co-occurrence partly explained by pleiotropic linkage of genetic locus identified on chromosome 11q23.1-q23.2 and comprises the gene sequence nuclear cell adhesion molecule 1-tetratricopeptide repeat domain 12-ankyrin repeat and kinase domain containing 1-dopamine receptor D2 (NCAM1-TTC12-ANKK1-DRD2). The relationship between the two is not invariant and is influenced by polymorphic DRD, endocannabinoid receptor (CNR), and 5-HT genes. Anhedonia seemed to be the most important symptom. Cannabinoid-induced long-term neuroplastic changes, particularly in the dorsal striatum, is a possible mechanism resulting in anhedonia and long-term effects on motivation.
大麻使用量的不断增加可能与动机降低和快感缺乏有关,而这两种症状都是抑郁症的表现。有阈下抑郁症状(如动机降低)的青少年大麻使用者除了情感发育受损外,还可能易患严重的快感缺乏。在大麻使用背景下,抑郁症的主要问题在于这两个变量之间是否存在神经生物学基础。使用关键词“大麻、抑郁症、青少年、内源性大麻素和气质”在医学主题词(MeSH)功能的PubMed数据库中进行搜索,共检索到1109篇文章。纳入的数据来自符合以下标准的研究:(i)在过去10年内发表(根据相关性纳入较旧的研究),(ii)针对青少年受试者(动物或人类),(iii)以英文发表,(iv)期刊文章、系统评价、荟萃分析、临床试验、观察性研究(动物或人类),(v)针对患有单相抑郁症且无合并症的受试者,以及(vi)针对使用大麻的受试者[无乙醇、尼古丁、可卡因、麦角酸二乙酰胺(LSD)和海洛因等混杂变量;且无合并精神病、躁狂或自闭症等医疗状况]。大麻素使用者的抑郁症状是一种常见的共病现象,部分原因可由11号染色体q23.1 - q23.2上鉴定的基因座的多效性连锁来解释,该基因座包含核细胞粘附分子1 - 四肽重复结构域12 - 锚蛋白重复序列和激酶结构域包含1 - 多巴胺受体D2(NCAM1 - TTC12 - ANKK1 - DRD2)的基因序列。两者之间的关系并非一成不变,而是受多态性多巴胺受体D(DRD)、内源性大麻素受体(CNR)和5 - 羟色胺(5 - HT)基因的影响。快感缺乏似乎是最重要的症状。大麻素诱导的长期神经可塑性变化,尤其是在背侧纹状体中的变化,是导致快感缺乏和对动机产生长期影响的一种可能机制。