中核accumbens D1和D2表达神经元控制食和活动介导的能量消耗之间的平衡
Roman Walle1, Anna Petitbon2, Giulia R Fois3
1Université de Bordeaux, INRAE, Bordeaux INP, NutriNeuro, 33000, Bordeaux, France. roman.walle@live.fr.
Nature communications
|March 22, 2024
概括
核 (NAc) 神经元的调节失调会影响饮食障碍 (ED). 在NAc核心中操纵多巴胺D1和D2受体表达神经元影响了食,运动和能量平衡,为ED病变产生提供了新的见解.
科学领域:
- 神经科学是一个神经科学.
- 行为神经科学 行为神经科学
- 内分泌学 在内分泌学.
背景情况:
- 腹核 (NAc) 涉及饮食障碍 (ED),但其在ED维度中的具体作用尚未完全理解.
- 在NAc中的多巴胺受体表达神经元对于奖励处理和动机行为至关重要,包括食和运动.
研究的目的:
- 研究NAc核心中多巴胺D1和D2受体表达神经元对养行为,运动和能量平衡的不同作用.
- 探索针对这些神经元子群的潜力,以治疗饮食障碍的治疗干预.
主要方法:
- 在雄性小鼠中使用化学基因操纵来选择性地激活或抑制NAc核心中多巴胺D1和D2受体表达神经元.
- 行为测试用于测量食物奖励的努力,自愿运动和食物摄入量.
- 在慢性操纵条件下监测身体重量和能量平衡.
主要成果:
- 激活NAc核心D1神经元增加了食物奖励和运动的努力,同时减少了食物摄入量.
- 相反,NAc核心D2神经元的激活显示出相反的效果,减少了努力,增加了食物摄入量.
- 慢性操纵策略,特别是D1激活与D2抑制的结合,显著改变了能量消耗和摄入量,D1激活/D2抑制在厌食症模型中加速减肥.
结论:
- 对NAc多巴胺受体神经元的调节失调,特别是D1和D2亚群,可能是饮食障碍的核心症状的基础.
- 准NAc D1和D2神经元为治疗饮食障碍和相关代谢失调提供了潜在的治疗途径.
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