Addiction is a debilitating condition that extracts enormous social and economic tolls. Despite several decades of research, our knowledge of its etiology, preventive measures, and treatments is limited. A relatively recent research field with the potential to provide a more holistic understanding, and subsequently treatments, takes a phylogenetic view of addiction. This perspective is based on deep homologies at the genetic, proteomic, and behavioral levels, which are shared across all metazoan life; particularly those organisms faced with plant secondary metabolites as defensive compounds against insect herbivory. These addictive alkaloids, such as nicotine, cocaine, or cathinone, are commonly referred to as “human drugs of abuse” even though humans had little to no role in the co-evolutionary processes that determined their initial emergence or continued selection. This commentary discusses the overwhelming homologies of addictive alkaloid effects on neural systems across a wide range of taxa, as we aim to develop a broader comparative view of the “addicted brain.” Taking nicotine as an example, homologous physiological responses to this compound identify common underlying cellular and molecular mechanisms that advocate for the adoption of a phylogenetic view of addiction.
Brain Behav Evol

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成瘾的深层根源：比较视角

成瘾是一种使人衰弱的疾病，会造成巨大的社会和经济损失。尽管进行了几十年的研究，但我们对其病因、预防措施和治疗的了解仍然有限。一个相对较新的研究领域有可能提供更全面的理解和随后的治疗，它采用了成瘾的系统发育观点。这种观点基于遗传、蛋白质组学和行为水平的深层同源性，这些在所有后生动物生命中都是相同的；特别是那些面临植物次生代谢物作为防御昆虫食草动物的化合物的生物。这些令人上瘾的生物碱，如尼古丁、可卡因或卡西酮，尽管人类在决定它们最初出现或继续选择的共同进化过程中几乎没有作用，但它们通常被称为“人类滥用药物”。这篇评论讨论了成瘾性生物碱对广泛分类群的神经系统影响的压倒性同源性，因为我们的目标是对“成瘾大脑”进行更广泛的比较。以尼古丁为例，对这种化合物的同源生理反应确定了共同的潜在细胞和分子机制，这些机制提倡采用成瘾的系统发育观点。
大脑行为进化