Traditional theories of neuroeconomics focus on reinforcement learning and reward value. We propose here a novel reframing of reinforcement learning and motivation that includes a hippocampal-dependent regulatory mechanism which balances cue-induced behavioral excitation with behavioral inhibition. This mechanism enables interoceptive cues produced by respective food or drug satiety to antagonize the ability of excitatory food- and drug-related environmental cues to retrieve the memories of food and drug reinforcers, thereby suppressing the power of those cues to evoke appetitive behavior. When the operation of this mechanism is impaired, ability of satiety signals to inhibit appetitive behavior is weakened because the relative balance between inhibition and simple excitation is shifted toward increased retrieval of food and drug memories by environmental cues. In the present paper, we (1) describe the associative processes that constitute this mechanism of hippocampal-dependent behavior inhibition; (2) describe how a prevailing obesity-promoting diet and drugs of abuse produce hippocampal pathophysiologies that can selectively impair this inhibitory function; and (3) propose how glucagon-like peptide 1 (GLP-1), an incretin hormone that is recognized as an important satiety signal, may work to protect the hippocampal-dependent inhibition. Our perspective may add to neuroscientific and neuroeconomic analyses of both overeating and drug abuse by outlining the role of hippocampal-dependent memory processes in the control of both food and drug seeking behaviors. In addition, this view suggests that consideration should be given to diet- and drug induced hippocampal pathophysiologies, as potential novel targets for the treatment of dysregulated energy and drug intake.

中文翻译：

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将食欲强化学习和奖励评估重新定义为海马依赖性行为抑制介导的影响

神经经济学的传统理论侧重于强化学习和奖励价值。我们在这里提出了一种新的强化学习和动机重构，其中包括一种海马依赖性调节机制，该机制可以平衡线索诱导的行为兴奋和行为抑制。这种机制使由各自的食物或药物饱腹感产生的内感受性线索能够对抗兴奋性食物和药物相关环境线索检索食物和药物强化剂记忆的能力，从而抑制这些线索唤起食欲行为的能力。当这个机制的运作受到损害时，饱腹感信号抑制食欲行为的能力减弱，因为抑制和简单兴奋之间的相对平衡转向通过环境线索增加食物和药物记忆的检索。在本文中，我们（1）描述了构成这种海马依赖性行为抑制机制的联想过程；(2) 描述流行的促进肥胖的饮食和滥用药物如何产生可以选择性地损害这种抑制功能的海马病理生理学；(3) 提出胰高血糖素样肽 1 (GLP-1)（一种被认为是重要的饱腹感信号的肠促胰岛素激素）如何保护海马依赖性抑制。通过概述海马依赖性记忆过程在控制食物和药物寻求行为中的作用，我们的观点可能会增加对暴饮暴食和药物滥用的神经科学和神经经济学分析。此外，这种观点表明应该考虑饮食和药物诱导的海马病理生理学，作为治疗能量和药物摄入失调的潜在新靶点。