GLP-1 influences food and drug reward.
GLP-1 influences food and drug reward.
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DOI：
10.1016/j.cobeha.2016.02.005
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发表时间：
2016-06
影响因子：
5
通讯作者：
Schmidt HD
中科院分区：
文献类型：
--
作者：
Hayes MR;Schmidt HD
自然奖励，包括食物，水，睡眠和社会互动，是维持生命所必需的。调节这些行为的强化效应的神经基质也是调节情绪、动机和药物刺激的奖励效应的相同神经生物学机制。神经肽胰高血糖素样肽-1（GLP-1）正在研究中的进食的稳态和享乐控制并不令人惊讶或新颖。然而，如果强调食物奖励的神经基质通常与其他奖励相关行为共享，那么未来的研究应该调查并接受内源性和外源性GLP-1受体激活可能影响多种奖励相关行为的可能性。事实上，对动机性进食行为背后的神经生物学机制的研究，已经为药物成瘾的神经基础研究提供了很多信息。一个新兴的文献表明GLP-1系统在调节适应不良的奖励行为，包括药物和酒精消费的作用。因此，如果基于GLP-1的药物疗法用于治疗药物成瘾和与适应不良奖励行为相关的其他疾病（例如肥胖和进食障碍），神经科学领域必须对脑内每个GLP-1受体表达核进行系统的、机制性神经药理学和行为研究。这些研究可能导致行为选择性，这可能为未来靶向离散脑核团中GLP-1 R信号传导以治疗动机性行为的方法提供信息。同样可能的是，在基于GLP-1的药物治疗中可能观察到对自然奖励和适应不良奖励行为的非选择性影响。在这种情况下，更好地了解中枢GLP-1 R激活增加对动机行为的影响将有助于治疗异常进食行为和/或药物依赖的临床方法。
Natural rewards, including food, water, sleep and social interactions, are required to sustain life. The neural substrates that regulate the reinforcing effects of these behaviors are also the same neurobiological mechanisms mediating mood, motivation and the rewarding effects of pharmacological stimuli. That the neuropeptide glucagon-like peptide-1 (GLP-1) is under investigation for both the homeostatic and hedonic controls of feeding is not surprising or novel. However, if the neural substrates that underline food reward are shared with other reward-related behaviors generally, then future research should investigate and embrace the likelihood that endogenous and exogenous GLP-1 receptor activation may influence multiple reward-related behaviors. Indeed, studies of the neurobiological mechanisms underlying motivated feeding behavior have informed much of the basic research investigating neural substrates of drug addiction. An emerging literature demonstrates a role for the GLP-1 system in modulating maladaptive reward behaviors, including drug and alcohol consumption. Thus, if GLP-1-based pharmacotherapies are to be used to treat drug addiction and other diseases associated with maladaptive reward behaviors (e.g. obesity and eating disorders), the neuroscience field must conduct systematic, mechanistic neuropharmacological and behavioral studies of each GLP-1 receptor-expressing nucleus within the brain. It is possible that behavioral selectivity may result from these studies, which could inform future approaches to targeting GLP-1R signaling in discrete brain nuclei to treat motivated behaviors. Equally as likely, non-selective effects on natural reward and maladaptive reward behaviors may be observed for GLP-1-based pharmacotherapies. In this case, a better understanding of the effects of increased central GLP-1R activation on motivated behaviors will aid in clinical approaches toward treating aberrant feeding behaviors and/or drug dependence.