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Author Notes:

Correspondence: Stephan Kratzer, s.kratzer@tum.de

SK designed and performed experiments, wrote manuscript;

CM performed experiments and provided critical feedback on manuscript

SS, EK, PG, GS, and GR provided critical feedback on the manuscript

RH designed experiments and provided critical feedback on manuscript

MK designed and conducted analysis, wrote manuscript.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


Research Funding:

This work was funded by institutional funding (Kommission klinische Forschung der TU Muenchen, KKF-B to SK).

This work was supported by the German Research Foundation (DFG) and the Technical University of Munich (TUM) in the framework of the Open Access Publishing Program.

A portion of the research efforts from MK and PG were supported by funding from the James S. McDonnell Foundation (www.jsmf.org).

PG research efforts are also supported by funding from the Veteran's Administration (BX001677).


  • Science & Technology
  • Life Sciences & Biomedicine
  • Mathematical & Computational Biology
  • Neurosciences
  • Neurosciences & Neurology
  • propofol
  • sevoflurane
  • thalamocortical
  • unconsciousness
  • mechanisms of anesthesia

Propofol and Sevoflurane Differentially Modulate Cortical Depolarization following Electric Stimulation of the Ventrobasal Thalamus


Journal Title:

Frontiers in Computational Neuroscience


Volume 11


Type of Work:

Article | Final Publisher PDF


The neuronal mechanisms how anesthetics lead to loss of consciousness are unclear. Thalamocortical interactions are crucially involved in conscious perception; hence the thalamocortical network might be a promising target for anesthetic modulation of neuronal information pertaining to arousal and waking behavior. General anesthetics affect the neurophysiology of the thalamus and the cortex but the exact mechanisms of how anesthetics interfere with processing thalamocortical information remain to be elucidated. Here we investigated the effect of the anesthetic agents sevoflurane and propofol on thalamocortical network activity in vitro. We used voltage-sensitive dye imaging techniques to analyze the cortical depolarization in response to stimulation of the thalamic ventrobasal nucleus in brain slices from mice. Exposure to sevoflurane globally decreased cortical depolarization in a dose-dependent manner. Sevoflurane reduced the intensity and extent of cortical depolarization and delayed thalamocortical signal propagation. In contrast, propofol neither affected area nor amplitude of cortical depolarization. However, propofol exposure resulted in regional changes in spatial distribution of maximum fluorescence intensity in deep regions of the cortex. In summary, our experiments revealed substance-specific effects on the thalamocortical network. Functional changes of the neuronal network are known to be pivotally involved in the anesthetic-induced loss of consciousness. Our findings provide further evidence that the mechanisms of anesthetic-mediated loss of consciousness are drug- and pathway-specific.

Copyright information:

© 2017 Kratzer, Mattusch, Garcia, Schmid, Kochs, Rammes, Schneider, Kreuzer and Haseneder.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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