Activation of Dopamine Signals in the Olfactory Tubercle Facilitates Emergence from Isoflurane Anesthesia in Mice

Activation of Dopamine Signals in the Olfactory Tubercle Facilitates Emergence from Isoflurane Anesthesia in Mice
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嗅结节中多巴胺信号的激活促进小鼠从异氟醚麻醉中苏醒

DOI:
10.1007/s11064-021-03291-4
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发表时间:
2021-03-12
影响因子:
4.4
通讯作者:
Xu,Haibo
Xu,Haibo
中科院分区:
医学3区
文献类型:
--
作者:
Yang,Bo;Ao,Yawen;Xu,Haibo

文献摘要

相似文献

多巴胺(DA)神经元的激活对于从睡眠到觉醒的过渡和维持觉醒是必不可少的,并且足以加速动物从全身麻醉中苏醒。多巴胺受体(Dopamine receptor,DR)参与唤醒的调节。在本研究中,我们发现嗅结节(OT)在异氟醚麻醉苏醒期间是活跃的,局部注射多巴胺D1受体(D1 R)激动剂氯-APB(1 mg/mL)和D2受体(D2 R)激动剂喹吡罗(1 mg/mL)到OT中增强异氟醚麻醉的行为和皮层唤醒,D1 R拮抗剂SCH-23390(1 mg/mL)和D2 R拮抗剂雷氯必利(2.5 mg/mL)可延长恢复时间。OT中DA能末梢的光遗传激活也促进了异氟烷麻醉的行为和皮质唤醒。D1 R/D2 R激动剂和D1 R/D2 R拮抗剂对异氟醚麻醉诱导无影响。OT中DA能末梢的光遗传刺激对麻醉诱导也没有影响。我们的研究结果表明,DA信号OT加速异氟醚麻醉的出现。此外,与苏醒过程不同,全身麻醉的诱导不是由OT DA能通路介导的。
Activation of dopamine (DA) neurons is essential for the transition from sleep to wakefulness and maintenance of awakening, and sufficient to accelerate the emergence from general anesthesia in animals. Dopamine receptors (DR) are involve in arousal mediation. In the present study, we showed that the olfactory tubercle (OT) was active during emergence from isoflurane anesthesia, local injection of dopamine D1 receptor (D1R) agonist chloro-APB (1 mg/mL) and D2 receptor (D2R) agonist quinpirole (1 mg/mL) into OT enhanced behavioural and cortical arousal from isoflurane anesthesia, while D1R antagonist SCH-23390 (1 mg/mL) and D2R antagonist raclopride (2.5 mg/mL) prolonged recovery time. Optogenetic activation of DAergic terminals in OT also promoted behavioural and cortical arousal from isoflurane anesthesia. However, neither D1R/D2R agonists nor D1R/D2R antagonists microinjection had influences on the induction of isoflurane anesthesia. Optogenetic stimulation on DAergic terminals in OT also had no impact on the anesthesia induction. Our results indicated that DA signals in OT accelerated emergence from isoflurane anesthesia. Furthermore, the induction of general anesthesia, different from the emergence process, was not mediated by the OT DAergic pathways.