Signatures of Thalamocortical Alpha Oscillations and Synchronization With Increased Anesthetic Depths Under Isoflurane

• Published in: Frontiers in pharmacology Vol. 13; p. 887981
• Main Authors: Jiang, Jingyao, Zhao, Yi, Liu, Jin, Yang, Yaoxin, Liang, Peng, Huang, Han, Wu, Yongkang, Kang, Yi, Zhu, Tao, Zhou, Cheng
• Format: Journal Article
• Language: English
• Published: Frontiers Media S.A 03.06.2022
• Subjects: alpha oscillations; computational model; electroencephalogram; isoflurane; Pharmacology; phase–amplitude coupling; thalamocortical networks
• ISSN: 1663-9812; 1663-9812
• DOI: 10.3389/fphar.2022.887981

Background: Electroencephalography (EEG) recordings under propofol exhibit an increase in slow and alpha oscillation power and dose-dependent phase–amplitude coupling (PAC), which underlie GABA A potentiation and the central role of thalamocortical entrainment. However, the exact EEG signatures elicited by volatile anesthetics and the possible neurophysiological mechanisms remain unclear. Methods: Cortical EEG signals and thalamic local field potential (LFP) were recorded in a mouse model to detect EEG signatures induced by 0.9%, 1.5%, and 2.0% isoflurane. Then, the power of the EEG spectrum, thalamocortical coherence, and slow–alpha phase–amplitude coupling were analyzed. A computational model based on the thalamic network was used to determine the primary neurophysiological mechanisms of alpha spiking of thalamocortical neurons under isoflurane anesthesia. Results: Isoflurane at 0.9% (light anesthesia) increased the power of slow and delta oscillations both in cortical EEG and in thalamic LFP. Isoflurane at 1.5% (surgery anesthesia) increased the power of alpha oscillations both in cortical EEG and in thalamic LFP. Isoflurane at 2% (deep anesthesia) further increased the power of cortical alpha oscillations, while thalamic alpha oscillations were unchanged. Thalamocortical coherence of alpha oscillation only exhibited a significant increase under 1.5% isoflurane. Isoflurane-induced PAC modulation remained unchanged throughout under various concentrations of isoflurane. By adjusting the parameters in the computational model, isoflurane-induced alpha spiking in thalamocortical neurons was simulated, which revealed the potential molecular targets and the thalamic network involved in isoflurane-induced alpha spiking in thalamocortical neurons. Conclusion: The EEG changes in the cortical alpha oscillation, thalamocortical coherence, and slow–alpha PAC may provide neurophysiological signatures for monitoring isoflurane anesthesia at various depths.