Abstract SNACC-19

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Propofol and sevoflurane differentially modulate cortical processing of thalamic signals – results from voltage-sensitive dye imaging in vitro

Kratzer S, Kreuzer M, Kochs E, Gerhard R, Haseneder R
Klinikum rechts der Isar der TU Muenchen, Muenchen, Bavaria, Germany

Background: Sensory information from the thalamus undergoes basic signal transformation in a cortical column before its trans-columnar integration across cortical areas (1). Therefore, vertical as well as longitudinal circuits in the cortex are potential targets for anesthetics. We investigated the effect of propofol and sevoflurane (sev) on thalamocortical (TC) activity propagation in murine brain slices.

Materials and Methods: TC brain slices (Bl6 mice, p28-42) were prepared and stained with the voltage-sensitive dye Di-4-ANEPPS (7.5 mg/ml; < 0.1% DMSO). Signals were evoked by electrical stimulation of the ventrobasal thalamus. A pixel range was selected either along the cortex (longitudinal) or through the layers of the cortex (vertical). Level of fluorescence for each pixel was recorded and analyzed for the duration of 220 ms (100 frames) after stimulation. The following parameters were analyzed: Time point and intensity value of the maximum fluorescence-intensity of each selected pixel as well as the maximum intensity value and its location for each of the 100 frames. After stable baseline recordings, propofol (1 µM) was added to the aCSF or the perfusion medium was saturated with 3.2 % sev. Hedges’ g (2) was used for statistic evaluation of parameter changes.

Results: In vertical pixel selections, sev reduced the maximum intensity from 4.9±0.8 to 3.7±0.6 (Hedges’ g: 0.72 CI: [-0.09 1.97]) and prolonged the time of TC signal transmission from 35.4±5.9 ms to 51.5±7.8 ms (Hedges’ g: -0.94 CI [-3.38 -0.11]). In contrast, propofol neither affected the intensity nor the temporal delay of TC transmission.
Regarding longitudinal signal propagation, propofol reduced the maximum intensity from 4.8±0.5 to 3.9±0.4 (Hedges’ g: 0.8 CI [0.34 1.92]). Analogously, sev decreased the maximum fluorescence-intensity along the cortex from 6.5±1.3 to 3.6±0.4 (Hedges’ g: 1.25 CI [1.04 4.78]). Interestingly, propofol affected horizontal cortical signal processing as the maximum intensities were spread over considerably more pixels (26.7±1.4) than at control conditions (20.0±2.5 pixels; Hedges’ g -1.25 CI [-2.8 -0.3]) whereas sev did not affect this spatial distribution.

Conclusion(s): We show how propofol and sev differentially affect cortical processing of thalamic inputs. From a functional point of view, vertical pixel selections through the cortical layers reflect the first level of cortical processing of thalamic input (3). Sev prolonged TC signal transmission and thus impaired early cortical processing. The longitudinal propagation of sensory signals across large areas of the cortex reflects integrative processing (4). Hence, longitudinal pixel selections rather represent integrative cortical activity. The propofol-mediated change in longitudinal spread of maxima might therefore reflect altered cortical integration of sensory information. In summary, our results suggest, that sev affects initial cortical processing of thalamic inputs whereas propofol impacts integrative computing.

References: 1. Lübke J, et al. Brain Struct Funct. 2007; 2. Hentschke H, et al. Eur J Neurosci. 2011; 3. Hill M, et al. Frontiers in Neuroscience 2014; 4. Feldmeyer D, et al. Prog Neurobiol. 2013

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