前额叶皮层到下丘脑的输出通过AMPKβ2信号,通过暗示器增强的可口食物消费进行编排
Jiakun Xiang1, Minghong Shi1, Jiajia Kang1
1Shanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Brain Function and Disorders and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China.
认知线索驱动过度饮食和肥胖. 研究人员发现,前临床皮质 (PrL) 中的AMPKβ2调节了这种反应,为饮食障碍治疗提供了潜在的目标.
科学领域:
- 神经科学是一个神经科学.
- 代谢研究研究 代谢研究
- 肥胖研究 肥胖研究
背景情况:
- 认知因素显著影响食欲和食物摄入量,在肥胖环境中导致肥胖.
- 连接认知影响与过度消费的精确细胞和分子机制尚不清楚.
研究的目的:
- 研究神经机制,通过学习环境线索引发过度消费高脂肪饮食 (HFD).
- 识别参与HFD相关学习和提示驱动的养行为中的分子参与者.
主要方法:
- 在自由移动的小鼠中进行成像,以监测前临床皮质 (PrL) 中的神经元活动.
- 转录组分析以识别HFD相关学习后PrL中的分子变化.
- 基因操纵以评估AMPKβ2和PrL神经元投射的作用.
主要成果:
- 前皮质 (PrL) 神经元表现出可塑性,以响应与HFD配对的学习线索,预测消费持续时间.
- 与HFD相关的学习改变了PrL中的ATP代谢过程.
- AMPKβ2的枯竭破坏了PrL的可塑性,并防止了提示驱动的HFD过度消耗.
- PrL投射到横向下丘脑的奥雷克辛神经元对于有条件的HFD过度消费至关重要.
结论:
- 一个涉及PrL和素神经元的皮质-海波质路径调节了提示引起的HFD过度消费.
- 在调解PrL可塑性和与HFD相关的养行为方面,AMPKβ2起着至关重要的作用.
- AMPKβ2成为饮食障碍和肥胖症的潜在治疗标.
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