Dopamine D1 receptor in ventrolateral periaqueductal gray modulates propofol anesthesia in rats
10.16571/j.cnki.1008-8199.2020.08.002
- VernacularTitle: 腹外侧中脑导水管灰质多巴胺受体参与丙泊酚麻醉的作用研究
- Author:
Yi ZHANG
1
;
Yin-yin YANG
2
;
Yi-qiang XIONG
2
;
Qing PU
2
;
Yan-fei ZHAO
2
;
Cheng-xi LIU
2
Author Information
1. Department of Anesthesiology, the Second Affiliated Hospital of Zunyi Medical University, Zunyi 563000,Guizhou,China
2. Department of Anesthesiology, Guizhou Key Laboratory of Anesthesia and Organ Protection,Zunyi Medical University,Zunyi 563000,Guizhou,China
- Publication Type:Journal Article
- Keywords:
ventrolateral periaqueductal gray;
propofol;
dopamine D1 receptor;
dopamine D2 receptor;
calcium fiber photometry recording
- From:
Journal of Medical Postgraduates
2020;33(8):792-796
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveVentrolateral periaqueductal gray (vlPAG) locates in ascending reticular activating system, which plays a key role in the sleep-wake circle. However, the role of vlPAG in general anesthesia has not been identified. To investigate the effect of the dopamine receptor in vlPAG neurons on propofol anesthesia, we used real-time in vivo fiber photometry, microinjection and EEG.MethodsTo observe the alteration of neuronal activity in the vlPAG throughout propofol anesthesia, 10 Sprague-Dawley rats were used for calcium fiber photometry recording. 50 vlPAG bilateral microinjection models were established and assigned into five groups randomly, including D1R agonist group, D1R antagonist group, D2R agonist group, D2R antagonist group, and control group (n=10). Under propofol anesthesia, 1 μL of D1R agonist, D1R antagonist, D2R agonist, D2R antagonist, and isotonic saline were microinjected into the vlPAG of animals in the corresponding groups, respectively. The induction time, recovery time and the changes in electroencephalogram (EEG) before and after microinjection were recorded and analyzed.ResultsThe neuronal activity in the vlPAG was significantly inhibited during the induction period and markedly recovered during the recovery period from propofol anesthesia (P<0.05). Subsequently, the microinjection of D1R agonist into the vlPAG notably prolonged the induction time and reduced the emergence time of propofol anesthesia with a decrease of δ-band ratio. While the microinjection of D1R antagonist accelerated the induction time and prolonged the emergence time of propofol anesthesia with an increase of δ-band ratio and a decrease in β-band ratio in cortical EEG (P<0.05). The induction and recovery time of D2R agonist /antagonist group did not differ with those of control group. As well, EEG before and after microinjection in D2R agonist /antagonist group did not different.ConclusionThese results indicate that vlPAG modulates the process of propofol anesthesia via D1R.
