D1 and D2 neurons in the nucleus accumbens enable positive and negative control over sugar intake in mice.

D1 and D2 neurons in the nucleus accumbens enable positive and negative control over sugar intake in mice.
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DOI:
10.1016/j.celrep.2023.112190
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发表时间:
2023-03-28
期刊:
影响因子:
8.8
通讯作者:
--
中科院分区:
生物学1区
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--
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虽然碳水化合物的消耗是生存所必需的,但它们强大的强化特性导致了全球范围内的肥胖。反过来,糖的过度消费揭示了大脑奖励系统在调节糖摄入量方面的重要作用。然而,奖赏回路中的不同细胞类型如何控制含糖食物的开始和结束仍然是难以捉摸的。在这里,我们确定了不同的神经核细胞类型,介导的化学感觉与餐后性质的甜味糖。具体来说,D1神经元通过与味觉神经节的专门连接来增强糖的摄入,而D2神经元通过与食欲抑制相关回路的解剖学连接来介导含糖膳食的终止。一致的是,D2,而不是D1,神经元部分介导的胰高血糖素样肽1(GLP-1)激动剂的饱足效应。因此,这些神经核细胞类型起着行为开关的作用,能够对糖的摄入进行积极与消极的控制。我们的研究有助于揭示糖过度消费的细胞和电路基板。Sandoval-Rodríguez等人发现了一种控制哺乳动物奖励系统中糖摄入的开关机制。腹侧纹状体中两种不同类型的多巴胺受体表达神经元分别驱动和限制热量糖的摄入。这种转换机制涉及到味觉回路与食欲抑制回路之间的不同解剖学联系。
Although the consumption of carbohydrates is needed for survival, their potent reinforcing properties drive obesity worldwide. In turn, sugar overconsumption reveals a major role for brain reward systems in regulating sugar intake. However, it remains elusive how different cell types within the reward circuitries control the initiation and termination of sugary meals. Here, we identified the distinct nucleus accumbens cell types that mediate the chemosensory versus postprandial properties of sweet sugars. Specifically, D1 neurons enhance sugar intake via specialized connections to taste ganglia, whereas D2 neurons mediate the termination of sugary meals via anatomical connections to circuits involved in appetite suppression. Consistently, D2, but not D1, neurons partially mediate the satiating effects of glucagon-like peptide 1 (GLP-1) agonists. Thus, these nucleus accumbens cell types function as a behavioral switch, enabling positive versus negative control over sugar intake. Our study contributes to unveiling the cellular and circuit substrates of sugar overconsumption. Sandoval-Rodríguez et al. identified a switch mechanism that controls sugar intake within the mammalian reward system. Two separate types of dopamine-receptor-expressing neuron in ventral striatum respectively drive and limit caloric sugar intake. The switch mechanism involves distinct anatomical connections to gustatory versus appetite-suppressing circuits.
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