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Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

The specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propo...

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Detalles Bibliográficos
Autores principales: Bastos, André M, Donoghue, Jacob A, Brincat, Scott L, Mahnke, Meredith, Yanar, Jorge, Correa, Josefina, Waite, Ayan S, Lundqvist, Mikael, Roy, Jefferson, Brown, Emery N, Miller, Earl K
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8079153/
https://www.ncbi.nlm.nih.gov/pubmed/33904411
http://dx.doi.org/10.7554/eLife.60824
Descripción
Sumario:The specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little or no spiking activity, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation ‘awakened’ anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.