Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Neuropharmacology. 2011 Dec;61(7):1123-8. doi: 10.1016/j.neuropharm.2011.02.028. Epub 2011 Mar 21.
Across species, the brain evolved to respond to natural rewards such as food and sex. These physiological responses are important for survival, reproduction and evolutionary processes. It is no surprise, therefore, that many of the neural circuits and signaling pathways supporting reward processes are conserved from Caenorhabditis elegans to Drosophilae, to rats, monkeys and humans. The central role of dopamine (DA) in encoding reward and in attaching salience to external environmental cues is well recognized. Less widely recognized is the role of reporters of the "internal environment", particularly insulin, in the modulation of reward. Insulin has traditionally been considered an important signaling molecule in regulating energy homeostasis and feeding behavior rather than a major component of neural reward circuits. However, research over recent decades has revealed that DA and insulin systems do not operate in isolation from each other, but instead, work together to orchestrate both the motivation to engage in consummatory behavior and to calibrate the associated level of reward. Insulin signaling has been found to regulate DA neurotransmission and to affect the ability of drugs that target the DA system to exert their neurochemical and behavioral effects. Given that many abused drugs target the DA system, the elucidation of how dopaminergic, as well as other brain reward systems, are regulated by insulin will create opportunities to develop therapies for drug and potentially food addiction. Moreover, a more complete understanding of the relationship between DA neurotransmission and insulin may help to uncover etiological bases for "food addiction" and the growing epidemic of obesity. This review focuses on the role of insulin signaling in regulating DA homeostasis and DA signaling, and the potential impact of impaired insulin signaling in obesity and psychostimulant abuse.
在不同物种中,大脑进化为对自然奖励(如食物和性)做出反应。这些生理反应对于生存、繁殖和进化过程至关重要。因此,许多支持奖励过程的神经回路和信号通路从秀丽隐杆线虫到果蝇,再到老鼠、猴子和人类都是保守的,这并不奇怪。多巴胺(DA)在编码奖励和为外部环境线索赋予显著性方面的核心作用是众所周知的。不太广为人知的是“内部环境”的报告者,特别是胰岛素,在调节奖励中的作用。胰岛素传统上被认为是调节能量稳态和进食行为的重要信号分子,而不是神经奖励回路的主要组成部分。然而,近几十年来的研究表明,DA 和胰岛素系统并非彼此孤立运作,而是共同协调参与消费行为的动机,并校准相关的奖励水平。已经发现胰岛素信号调节 DA 神经传递,并影响靶向 DA 系统的药物发挥其神经化学和行为效应的能力。鉴于许多滥用药物靶向 DA 系统,阐明多巴胺能以及其他大脑奖励系统如何受到胰岛素的调节将为开发针对药物和潜在食物成瘾的治疗方法创造机会。此外,更全面地了解 DA 神经传递和胰岛素之间的关系可能有助于揭示“食物成瘾”和肥胖症日益流行的病因基础。本综述重点介绍了胰岛素信号在调节 DA 动态平衡和 DA 信号中的作用,以及胰岛素信号受损在肥胖症和精神兴奋剂滥用中的潜在影响。