下丘脑POMC神经元促进大麻素诱导的食
Marco Koch1, Luis Varela2, Jae Geun Kim2
11] Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA [2] Institute of Anatomy, University of Leipzig, 04103 Leipzig, Germany.
大麻素受体1 (CB1R) 的激活令人惊地增加了下丘脑的亲opiomelanocortin (POMC) 神经元活动,促进食. 在大麻素驱动的养中,这种意想不到的POMC神经元作用涉及β-endorphin释放和线粒体适应.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
背景情况:
- 传统上已知,下丘脑的亲米兰皮质蛋白 (POMC) 神经元可以促进腹感.
- 大麻素受体1 (CB1R) 在食物摄入的中央调节中发挥着关键作用.
研究的目的:
- 为了研究POMC神经元在CB1R控制的食中对足小鼠的作用.
- 确定CB1R激活是否影响POMC神经元活动及其对养行为的影响.
主要方法:
- 使用化学激动剂来促进小鼠的CB1R活性.
- 采用专门由设计药物 (DREADDs) 激活的设计受体来操纵POMC神经元活动.
- 在全身和下丘脑中使用纳洛,一种阿片类受体对抗剂.
- 研究了对CB1R激活的反应中的线粒体适应.
主要成果:
- CB1R激活增加了食,并且矛盾的是,促进了POMC神经元活动.
- 通过DREADDs抑制POMC神经元减少了CB1R诱导的食,而激活则增强了它.
- CB1R激活选择性地增加了下丘脑 β-内啡释放,而不是α-黑色素细胞刺激激素.
- 纳洛阻断了CB1R诱导的食,阻断线粒体适应消除了CB1R的影响.
结论:
- POMC神经元在促进大麻素刺激的食方面发挥了以前未知的作用.
- 由CB1R驱动的养涉及β-endorphin的释放,需要特定的线粒体适应.
- 这项研究揭示了CB1R信号传递,POMC神经元和食调节之间的复杂相互作用.
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