Palomo Tomas, Kostrzewa R M, Beninger R J, Archer T
Servicio Psiquiátrico, Hospital Universitario 12 de Octubre, Avda. de Córdoba s/n, 28041 Madrid, Spain.
Neurotox Res. 2004;6(5):343-61. doi: 10.1007/BF03033309.
Factors that confer predisposition and vulnerability for alcoholism and other substance abuse disorders may be described usefully within the gene-environment interplay framework. Thus, it is postulated that heritability provides a major contribution not only to alcohol but also to other substances of abuse. Studies of evoked potential amplitude reduction have provided a highly suitable and testable method for the assessment of both environmentally-determined and heritable characteristics pertaining to substance use and dependence. The different personal attributes that may co-exist with parental influence or exist in a shared, monozygotic relationship contribute to the final expression of addiction. In this connection, it appears that personality disorders are highly prevalent co-morbid conditions among addicted individuals, and, this co-morbidity is likely to be accounted for by multiple complex etiological relationships, not least in adolescent individuals. Co-morbidity associated with deficient executive functioning may be observed too in alcohol-related aggressiveness and crimes of violence. The successful intervention into alcohol dependence and craving brought about by baclofen in both human and animal studies elucidates glutamatergic mechanisms in alcoholism whereas the role of the dopamine transporter, in conjunction with both the noradrenergic and serotonergic transporters, are implicated in cocaine dependence and craving. The role of the cannabinoids in ontogeny through an influence upon the expression of key genes for the development of neurotransmitter systems must be considered. Finally, the particular form of behaviour/characteristic outcome due to childhood circumstance may lie with biological, gene-based determinants, for example individual characteristics of monoamine oxidase (MAO) activity levels, thereby rendering simple predictive measures both redundant and misguiding.
在基因 - 环境相互作用框架内，可以有效地描述导致酒精中毒和其他物质滥用障碍易感性和脆弱性的因素。因此，据推测，遗传不仅对酒精，而且对其他滥用物质都有重大影响。诱发电位幅度降低的研究为评估与物质使用和依赖相关的环境决定因素和遗传特征提供了一种非常合适且可测试的方法。可能与父母影响共存或以共享的同卵关系存在的不同个人属性有助于成瘾的最终表现。在这方面，人格障碍在成瘾个体中似乎是高度普遍的共病情况，而且这种共病很可能是由多种复杂的病因关系造成的，尤其是在青少年个体中。在与酒精相关的攻击性和暴力犯罪中也可能观察到与执行功能缺陷相关的共病。巴氯芬在人类和动物研究中对酒精依赖和渴望的成功干预阐明了酒精中毒中的谷氨酸能机制，而多巴胺转运体与去甲肾上腺素能和血清素能转运体一起，与可卡因依赖和渴望有关。必须考虑大麻素通过影响神经递质系统发育的关键基因表达在个体发生中的作用。最后，由于童年环境导致的特定行为/特征结果可能取决于生物学的、基于基因的决定因素，例如单胺氧化酶（MAO）活性水平的个体特征，从而使简单的预测措施既多余又具有误导性。
