7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

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

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          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.

          Related collections

          Most cited references 49

          • Record: found
          • Abstract: found
          • Article: not found

          How inhibition shapes cortical activity.

          Cortical processing reflects the interplay of synaptic excitation and synaptic inhibition. Rapidly accumulating evidence is highlighting the crucial role of inhibition in shaping spontaneous and sensory-evoked cortical activity and thus underscores how a better knowledge of inhibitory circuits is necessary for our understanding of cortical function. We discuss current views of how inhibition regulates the function of cortical neurons and point to a number of important open questions. Copyright © 2011 Elsevier Inc. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Consciousness and anesthesia.

            When we are anesthetized, we expect consciousness to vanish. But does it always? Although anesthesia undoubtedly induces unresponsiveness and amnesia, the extent to which it causes unconsciousness is harder to establish. For instance, certain anesthetics act on areas of the brain's cortex near the midline and abolish behavioral responsiveness, but not necessarily consciousness. Unconsciousness is likely to ensue when a complex of brain regions in the posterior parietal area is inactivated. Consciousness vanishes when anesthetics produce functional disconnection in this posterior complex, interrupting cortical communication and causing a loss of integration; or when they lead to bistable, stereotypic responses, causing a loss of information capacity. Thus, anesthetics seem to cause unconsciousness when they block the brain's ability to integrate information.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Molecular and neuronal substrates for general anaesthetics.

              Although general anaesthesia has been of tremendous importance for the development of surgery, the underlying mechanisms by which this state is achieved are only just beginning to be understood in detail. In this review, we describe the neuronal systems that are thought to be involved in mediating clinically relevant actions of general anaesthetics, and we go on to discuss how the function of individual drug targets, in particular GABA(A)-receptor subtypes, can be revealed by genetic studies in vivo.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Comput Neurosci
                Front Comput Neurosci
                Front. Comput. Neurosci.
                Frontiers in Computational Neuroscience
                Frontiers Media S.A.
                1662-5188
                11 December 2017
                2017
                : 11
                Affiliations
                1Department of Anesthesiology, Klinikum rechts der Isar, Technische Universität München , Munich, Germany
                2Department of Anesthesiology, Emory University , Atlanta, GA, United States
                3Research Service, Atlanta VA Medical Center , Atlanta, GA, United States
                Author notes

                Edited by: Xiaoli Li, Beijing Normal University, China

                Reviewed by: Ewa Kublik, Nencki Institute of Experimental Biology (PAS), Poland; Zhenhu Liang, Yanshan University, China

                *Correspondence: Stephan Kratzer s.kratzer@ 123456tum.de

                †These authors have contributed equally to this work.

                Article
                10.3389/fncom.2017.00109
                5732174
                Copyright © 2017 Kratzer, Mattusch, Garcia, Schmid, Kochs, Rammes, Schneider, Kreuzer and Haseneder.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 5, Tables: 1, Equations: 0, References: 51, Pages: 10, Words: 7658
                Categories
                Neuroscience
                Original Research

                Neurosciences

                propofol, sevoflurane, thalamocortical, unconsciousness, mechanisms of anesthesia

                Comments

                Comment on this article