脑乳酸通过其受体G蛋白结合受体81参与催氧诱导的厌氧
Tian Yang1, Zejun Wang1, Junxia Li2
1Department of Frigid Zone Medicine, College of High Altitude Military Medicine, Army Medical University, Chongqing 400038, China; Key Laboratory of Extreme Environmental Medicine, Ministry of Education of China, Chongqing 400038, China; Key Laboratory of High Altitude Medicine, PLA, Chongqing 400038, China.
Neuroscience
|November 18, 2023
概括
缺氧会通过乳酸和GPR81信号在大脑中触发体温下降. 抑制乳酸生产或激活GPR81会影响低氧暴露期间的温度调节.
科学领域:
- 神经科学是一个神经科学.
- 生理学 生理学 生理学
- 生物化学 生物化学
背景情况:
- 缺氧诱导的厌氧,身体核心温度的降低,有着不清楚的机制.
- 乳酸盐是糖解的产物,可以通过G蛋白结合受体81 (GPR81) 影响神经元活动.
研究的目的:
- 为了研究中枢乳酸和GPR81在低氧诱导的厌氧中的作用,在老鼠模型中.
主要方法:
- 鼠被暴露于低氧 (11.1% O2).
- 测量了脑脊液 (CSF) 中的乳酸水平和身体核心温度 (Tcore).
- 二乙酸盐 (DCA) 或GPR81激动剂 (CHBA) 已通过脑内静脉注射.
- 免疫光染色评估了GPR81表达和神经元激活 (c-Fos).
主要成果:
- 缺氧增加了CSF乳酸,并降低了Tcore.
- DCA的使用降低了CSF乳酸,并阻止了Tcore的下降.
- GPR81激动剂 (CHBA) 在normoxia下降了Tcore.
- 缺氧增加了脑下垂体前视区域 (PO/AH) 的神经元激活,而这种激活被DCA减弱.
- 在PO/AH中,CHBA还增加了神经元激活.
结论:
- 中央乳酸和GPR81信号传递在缺氧诱导的厌氧中起着关键作用.
- 这一途径为低氧期间的温度调节机制提供了新的见解.
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