内源性阿片类药物通过胰岛皮质-密室通路促进压力诱导的暴饮暴食
Jingyi Chen1,2, Leandra Mangieri1,2, Sophia Mar1,3
1Center for the Neurobiology of Addiction, Pain and Emotion;Departments of Anesthesiology, Pharmacology, and Bioengineering, University of Washington, Seattle, WA, USA.
bioRxiv : the preprint server for biology
|June 25, 2024
概括
压力通过激活Claustrum中的迪诺芬/卡帕阿片类受体系统来驱动过度饮食. 这项研究揭示了压力诱导的过度饮食的新型神经通路,突出了内源性阿片类药物的作用.
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
- 神经药理学神经药理学
背景情况:
- 压力是暴饮暴食障碍的一个已知的因素.
- 压力诱导的暴饮暴食背后的神经机制在很大程度上是未知的.
- 迪诺芬 (dyn) /卡帕阿片类受体 (KOR) 系统调解压力诱导的无情感.
研究的目的:
- 为了研究诺芬/卡帕阿片类受体系统在压力诱导的暴饮暴食行为中的作用.
- 为了确定参与这种行为的特定神经回路.
主要方法:
- 建立了一种小鼠模型,用于压力诱导的像暴饮暴食的饮食行为.
- 使用全脑分析,局部药理学和基因操纵 (KOR删除) 在关节 (CLA).
- 采用了体内记录 (纤维光度) 和用单细胞成像的迪诺芬生物传感器 (Klight).
主要成果:
- 受到压力的小鼠表现出增加了可口食物 (高脂肪,高糖) 的摄入量.
- 在CLA中的KOR信号对于压力诱导的暴饮暴食至关重要.
- 在食期间观察到CLA内部的消抑制和局部色素调的减弱.
- 前部岛屿皮层 (aIC) 被确定为CLA的迪诺芬 afferents的来源.
结论:
- 这项研究揭示了CLA中的一种新的神经通路,由内源性阿片类药物调节,有助于导致压力诱导的暴饮暴食.
- 这些发现突出了诺芬/KOR系统在与压力相关的饮食行为神经生物学中的关键作用.
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