内大麻素系统
神经科学
平衡
利莫那班
能量稳态
脑刺激奖励
迷走神经
神经化学
机制(生物学)
奖励制度
生物
多巴胺
大麻素受体
心理学
受体
神经学
伏隔核
内分泌学
肥胖
哲学
认识论
生物化学
刺激
兴奋剂
作者
Chloé Berland,Julien Castel,Romano Terrasi,Enrica Montalban,Ewout Foppen,Claire Martin,Giulio G. Muccioli,Serge Luquet,Giuseppe Gangarossa
标识
DOI:10.1038/s41380-021-01428-z
摘要
The regulation of food intake, a sine qua non requirement for survival, thoroughly shapes feeding and energy balance by integrating both homeostatic and hedonic values of food. Unfortunately, the widespread access to palatable food has led to the development of feeding habits that are independent from metabolic needs. Among these, binge eating (BE) is characterized by uncontrolled voracious eating. While reward deficit seems to be a major contributor of BE, the physiological and molecular underpinnings of BE establishment remain elusive. Here, we combined a physiologically relevant BE mouse model with multiscale in vivo approaches to explore the functional connection between the gut-brain axis and the reward and homeostatic brain structures. Our results show that BE elicits compensatory adaptations requiring the gut-to-brain axis which, through the vagus nerve, relies on the permissive actions of peripheral endocannabinoids (eCBs) signaling. Selective inhibition of peripheral CB1 receptors resulted in a vagus-dependent increased hypothalamic activity, modified metabolic efficiency, and dampened activity of mesolimbic dopamine circuit, altogether leading to the suppression of palatable eating. We provide compelling evidence for a yet unappreciated physiological integrative mechanism by which variations of peripheral eCBs control the activity of the vagus nerve, thereby in turn gating the additive responses of both homeostatic and hedonic brain circuits which govern homeostatic and reward-driven feeding. In conclusion, we reveal that vagus-mediated eCBs/CB1R functions represent an interesting and innovative target to modulate energy balance and counteract food-reward disorders.
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