General anaesthetics induce tonic inhibition and modulate the gain of neural populations : a modeling study
© Hutt and Voegtlin; licensee BioMed Central Ltd. 2012
- Published: 16 July 2012
- Anaesthetic Agent
- General Anaesthetic
- Neural Population
- Tonic Inhibition
- Gain Modulation
Anaesthetic agents are known to affect extra-synaptic GABAergic receptors, which induce tonic inhibitory currents. Since these receptors are very sensitive to small concentrations of agents, they are supposed to play an important role in the underlying neural mechanism of general anaesthesia. Moreover anaesthetic agents modulate the encephalographic activity (EEG) of patients and hence show an effect on neural populations. To understand better the tonic inhibition effect in single neurons on neural populations modulating the EEG, the work considers a neural population in a steady-state and studies numerically and analytically the modulation of its population firing rate and the nonlinear gain with respect to different levels of tonic inhibition. We consider populations of both type-I and type-II neurons. The populations under study are heterogeneous involving distributions of firing thresholds and inhibitory conductances. The tonic inhibition introduces shunting action.
Summarizing, the present work has discovered an increase of the population firing threshold and a population gain modulation induced by tonic inhibition and presents a mathematical expression for the population firing rate. Since extra-synaptic receptors nduce tonic inhibition and are activated by several general anaesthetics, it is reasonable to reason that neural populations under anaesthetic action experience both effects. Consequently, we conclude that anaesthetics may both diminish the resting activity by shift of the firing threshold  and disrupts functionally neural circuits by increased population gain .
The research resulting to the presented work has received funding from the European Research Council under (FP7/2007- 2013) / ERC grant agreement n 257253.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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