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Attenuation of High-Frequency (50–200 Hz) Thalamocortical Electroencephalographic Rhythms by Isoflurane in Rats Is More Pronounced for the Thalamus Than for the Cortex

Plourde, Gilles MD; Reed, Sean J. MSc; Chapman, C. Andrew PhD

doi: 10.1213/ANE.0000000000001166
Anesthetic Pharmacology: Research Report

BACKGROUND: Thalamocortical electroencephalographic rhythms in gamma (30–80 Hz) and high-gamma (80–200 Hz) ranges have been linked to arousal and conscious processes. We have recently shown that propofol causes a concentration-dependent attenuation of the power of thalamocortical rhythms in the 50 to 200 Hz range and that this effect is far more pronounced for the thalamus. To determine whether similar attenuation occurs with other anesthetics, we characterized the concentration-effect relationship of the inhaled anesthetic isoflurane on the spectral power of these rhythms.

METHODS: Local field potentials were recorded from the barrel cortex and ventroposteromedial thalamic nucleus in 9 chronically instrumented rats to measure spectral power in the gamma/high-gamma range (30–200 Hz). Rats were placed in an airtight chamber and isoflurane was administered at 0.75%, 1.1%, and 1.5% concentrations. Spectral power was assessed during baseline, at the 3 isoflurane concentrations after 30 minutes for equilibration, and during recovery over 4 frequency bands (30–50, 51–75, 76–125, and 126–200 Hz). Unconsciousness was defined as sustained loss of righting reflex. Multiple linear regression was used to model the change in power (after logarithmic transformation) as a function of concentration and recording site. P values were corrected for multiple comparisons.

RESULTS: Unconsciousness occurred at the 1.1% concentration in all animals. Isoflurane caused a robust (P ≤ 0.008) linear concentration-dependent attenuation of cortical and thalamic power in the 30 to 200 Hz range. The concentration-effect slope for the thalamus was steeper than for the cortex in the 51 to 75 Hz (P = 0.029) and 76 to 200 Hz (P < 0.001) ranges but not for the 30 to 50 Hz range (P = 0.320). Comparison with our previously published propofol data showed that slope for cortical power was steeper with isoflurane than with propofol for all frequency bands (P = 0.033). For thalamic power, the slope differences between isoflurane and propofol were not statistically significant (0.087 ≤ P ≤ 0.599).

CONCLUSIONS: Isoflurane causes a concentration-dependent attenuation of the power of thalamocortical rhythms in the 30 to 200 Hz range, and this effect is more pronounced for the thalamus than for the cortex for frequencies >50 Hz. In comparison with propofol, isoflurane caused a greater attenuation in the cortex, but the effects on the thalamus were similar. Isoflurane and propofol cause common alterations of fast thalamocortical rhythms that may constitute an electrophysiologic signature of the anesthetized state.

Published ahead of print February 1, 2016

From the Department of Anesthesia, McGill University, Montréal, Canada.

Accepted for publication December 1, 2015.

Published ahead of print February 1, 2016

Funding: This work was funded in part by a grant to Dr. Chapman from the Natural Sciences and Engineering Research Council (NSERC) of Canada. Drs. Plourde and Chapman are members of the Center for Studies in Behavioral Neurobiology funded by the Fonds de Récherche du Québec-Santé (FRQS).

The authors declare no conflicts of interest.

Reprints will not be available from the authors.

Address correspondence to Gilles Plourde, MD, Department of Anesthesia, McGill University, Montreal Neurological Hospital, Room 548, 3801 University St., Montreal, QC, Canada H3A 2B4. Address e-mail to

© 2016 International Anesthesia Research Society