{"title":"[异丙酚麻醉下丘脑室旁核谷氨酸能神经元促进清醒]。","authors":"Chang Qin, Jingyan Gao, Bao Fu","doi":"10.3760/cma.j.cn121430-20241017-00850","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To determine whether the glutamatergic neurons in the paraventricular nucleus of the thalamus (PVT) is involved in the change of consciousness induced by propofol through a combination of behavioral and electroencephalography (EEG) recordings.</p><p><strong>Methods: </strong>Healthy male VGluT2-IRES-Cre mice aged 8-12 weeks were used in this experiment. (1) The glutamatergic neurons in the PVT was selectively damaged, and its effect on propofol anesthesia induction and recovery times as well as the energy of EEG in different frequency bands were observed. (2) Optogenetics was utilized to selectively activate or inhibit glutamatergic neurons in the PVT to assess their influence on anesthesia induction and recovery times under propofol as well as the energy of EEG in different frequency bands.</p><p><strong>Results: </strong>(1) Selective ablation of glutamatergic neurons in the PVT significantly delayed recovery from propofol anesthesia with statistical difference as compared with the control group (s: 409.43±117.49 vs. 273.71±51.52, P < 0.05), but had no significant effect on anesthesia induction time. During the recovery phase of propofol, selective ablation of glutamatergic neurons in the PVT exhibited higher α-wave (1-4 Hz) power and reduced β-wave (12-15 Hz) power as compared with the control group. (2) Optogenetic activation of glutamatergic neurons in the PVT significantly prolonged anesthesia induction time under propofol (s: 161.67±29.09 vs. 119.33±18.98, P < 0.05) while significantly shortening the recovery time from propofol anesthesia (s: 208.67±57.19 vs. 288.83±34.52, P < 0.05). During the induction phase of propofol, activation of glutamatergic neurons in PVT reduced α-wave and α-wave (8-12 Hz) power, while during the recovery phase, α-wave power significantly increased as compared with the control group. (3) Optogenetic inhibition of glutamatergic neurons in the PVT delayed recovery from propofol anesthesia (s: 403.50±129.06 vs. 252.83±45.31, P < 0.05), but had no significant effect on induction time. During both the induction phase and recovery phase of propofol, the optogenetic inhibition of glutamatergic neurons in the PVT exhibited increased α-wave power.</p><p><strong>Conclusion: </strong>Glutamatergic neurons in the PVT are involved in the regulation of propofol anesthesia recovery process.</p>","PeriodicalId":24079,"journal":{"name":"Zhonghua wei zhong bing ji jiu yi xue","volume":"37 2","pages":"140-145"},"PeriodicalIF":0.0000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Glutamatergic neurons in paraventricular nucleus of the thalamus promote wakefulness during propofol anesthesia].\",\"authors\":\"Chang Qin, Jingyan Gao, Bao Fu\",\"doi\":\"10.3760/cma.j.cn121430-20241017-00850\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To determine whether the glutamatergic neurons in the paraventricular nucleus of the thalamus (PVT) is involved in the change of consciousness induced by propofol through a combination of behavioral and electroencephalography (EEG) recordings.</p><p><strong>Methods: </strong>Healthy male VGluT2-IRES-Cre mice aged 8-12 weeks were used in this experiment. (1) The glutamatergic neurons in the PVT was selectively damaged, and its effect on propofol anesthesia induction and recovery times as well as the energy of EEG in different frequency bands were observed. (2) Optogenetics was utilized to selectively activate or inhibit glutamatergic neurons in the PVT to assess their influence on anesthesia induction and recovery times under propofol as well as the energy of EEG in different frequency bands.</p><p><strong>Results: </strong>(1) Selective ablation of glutamatergic neurons in the PVT significantly delayed recovery from propofol anesthesia with statistical difference as compared with the control group (s: 409.43±117.49 vs. 273.71±51.52, P < 0.05), but had no significant effect on anesthesia induction time. During the recovery phase of propofol, selective ablation of glutamatergic neurons in the PVT exhibited higher α-wave (1-4 Hz) power and reduced β-wave (12-15 Hz) power as compared with the control group. (2) Optogenetic activation of glutamatergic neurons in the PVT significantly prolonged anesthesia induction time under propofol (s: 161.67±29.09 vs. 119.33±18.98, P < 0.05) while significantly shortening the recovery time from propofol anesthesia (s: 208.67±57.19 vs. 288.83±34.52, P < 0.05). During the induction phase of propofol, activation of glutamatergic neurons in PVT reduced α-wave and α-wave (8-12 Hz) power, while during the recovery phase, α-wave power significantly increased as compared with the control group. (3) Optogenetic inhibition of glutamatergic neurons in the PVT delayed recovery from propofol anesthesia (s: 403.50±129.06 vs. 252.83±45.31, P < 0.05), but had no significant effect on induction time. During both the induction phase and recovery phase of propofol, the optogenetic inhibition of glutamatergic neurons in the PVT exhibited increased α-wave power.</p><p><strong>Conclusion: </strong>Glutamatergic neurons in the PVT are involved in the regulation of propofol anesthesia recovery process.</p>\",\"PeriodicalId\":24079,\"journal\":{\"name\":\"Zhonghua wei zhong bing ji jiu yi xue\",\"volume\":\"37 2\",\"pages\":\"140-145\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Zhonghua wei zhong bing ji jiu yi xue\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3760/cma.j.cn121430-20241017-00850\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhonghua wei zhong bing ji jiu yi xue","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3760/cma.j.cn121430-20241017-00850","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
摘要
目的:通过行为记录和脑电图记录相结合的方法,探讨丘脑室旁核谷氨酸能神经元是否参与异丙酚诱导的意识改变。方法:以8 ~ 12周龄健康雄性VGluT2-IRES-Cre小鼠为实验对象。(1)选择性损伤PVT内谷氨酸能神经元,观察其对异丙酚麻醉诱导、恢复时间及不同频带脑电能量的影响。(2)利用光遗传学技术选择性激活或抑制PVT内谷氨酸能神经元,评估其对异丙酚麻醉诱导和恢复时间以及不同频段脑电图能量的影响。结果:(1)选择性消融PVT谷氨酸能神经元显著延迟异丙酚麻醉后恢复,与对照组比较差异有统计学意义(s: 409.43±117.49∶273.71±51.52,P < 0.05),但对麻醉诱导时间无显著影响。在异丙酚恢复期,选择性消融PVT谷氨酸能神经元的α波(1 ~ 4 Hz)功率高于对照组,β波(12 ~ 15 Hz)功率低于对照组。(2)光遗传激活PVT谷氨酸能神经元显著延长丙泊酚麻醉诱导时间(s: 161.67±29.09 vs. 119.33±18.98,P < 0.05),显著缩短丙泊酚麻醉恢复时间(s: 208.67±57.19 vs. 288.83±34.52,P < 0.05)。异丙酚诱导期谷氨酸能神经元α-波和α-波(8 ~ 12 Hz)功率降低,恢复期α-波功率较对照组显著升高。(3)异丙酚麻醉后PVT恢复延迟(s: 403.50±129.06 vs. 252.83±45.31,P < 0.05),但对诱导时间无显著影响。在异丙酚诱导期和恢复期,PVT内谷氨酸能神经元的光遗传抑制表现为α-波功率增加。结论:PVT内谷氨酸能神经元参与异丙酚麻醉恢复过程的调节。
[Glutamatergic neurons in paraventricular nucleus of the thalamus promote wakefulness during propofol anesthesia].
Objective: To determine whether the glutamatergic neurons in the paraventricular nucleus of the thalamus (PVT) is involved in the change of consciousness induced by propofol through a combination of behavioral and electroencephalography (EEG) recordings.
Methods: Healthy male VGluT2-IRES-Cre mice aged 8-12 weeks were used in this experiment. (1) The glutamatergic neurons in the PVT was selectively damaged, and its effect on propofol anesthesia induction and recovery times as well as the energy of EEG in different frequency bands were observed. (2) Optogenetics was utilized to selectively activate or inhibit glutamatergic neurons in the PVT to assess their influence on anesthesia induction and recovery times under propofol as well as the energy of EEG in different frequency bands.
Results: (1) Selective ablation of glutamatergic neurons in the PVT significantly delayed recovery from propofol anesthesia with statistical difference as compared with the control group (s: 409.43±117.49 vs. 273.71±51.52, P < 0.05), but had no significant effect on anesthesia induction time. During the recovery phase of propofol, selective ablation of glutamatergic neurons in the PVT exhibited higher α-wave (1-4 Hz) power and reduced β-wave (12-15 Hz) power as compared with the control group. (2) Optogenetic activation of glutamatergic neurons in the PVT significantly prolonged anesthesia induction time under propofol (s: 161.67±29.09 vs. 119.33±18.98, P < 0.05) while significantly shortening the recovery time from propofol anesthesia (s: 208.67±57.19 vs. 288.83±34.52, P < 0.05). During the induction phase of propofol, activation of glutamatergic neurons in PVT reduced α-wave and α-wave (8-12 Hz) power, while during the recovery phase, α-wave power significantly increased as compared with the control group. (3) Optogenetic inhibition of glutamatergic neurons in the PVT delayed recovery from propofol anesthesia (s: 403.50±129.06 vs. 252.83±45.31, P < 0.05), but had no significant effect on induction time. During both the induction phase and recovery phase of propofol, the optogenetic inhibition of glutamatergic neurons in the PVT exhibited increased α-wave power.
Conclusion: Glutamatergic neurons in the PVT are involved in the regulation of propofol anesthesia recovery process.