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GENERAL ARTICLES

Local GABA_A Receptor Blockade Reverses Isoflurane’s Suppressive Effects on Thalamic Neurons In Vivo

Christiane Vahle-Hinz, PhD^*, Oliver Detsch, MD, Matthias Siemers, MSc^*, Eberhard Kochs, MD, and Burkhart Bromm, MD, PhD^*

*Institut für Physiologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany; and Klinik für Anaesthesiologie, Klinikum rechts der Isar, Technische Universität München, Munich, Germany

Address correspondence and reprint requests to Dr. Christiane Vahle-Hinz, Institut für Physiologie, Universitätsklinikum Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany. Address e-mail to vahle{at}uke.uni-hamburg.de

Many in vitro effects of volatile anesthetics are known, but the mechanisms of action are still under debate. Because suppression of sensory perception is one of the major goals of general anesthesia, we studied the effects of isoflurane on the processing of somatosensory information in anesthetized rats. Local iontophoretic administration of the -aminobutyric acid-A (GABA_A) receptor antagonist bicuculline in the thalamic ventral posteromedial nucleus reversed suppressive effects of isoflurane on thalamocortical relay neurons (TCNs). The action potential discharges of TCNs (n = 23) in response to defined mechanical stimulation of receptive fields seen with small concentrations of isoflurane (0.79% ± 0.01%, mean ± SEM) were suppressed under large concentrations (1.44% ± 0.04%). In addition, the tonic response pattern was lost, which initially encoded the information about the stimulus features. In 70% of TCNs, bicuculline administration reestablished the initially present tonic response pattern under large isoflurane concentrations. These results indicate that isoflurane suppresses somatosensory information transfer at the thalamic level in vivo, apparently by enhancing thalamic GABA_A receptor-mediated inhibition.

Implications: Isoflurane actions in the thalamus suppressed the transmission of tactile input to the cortex. This effect was reversed by removal of thalamic inhibition. Suppression of sensory perception under general anesthesia, therefore, may result in part from isoflurane’s interaction with thalamic -aminobutyric acid-A receptors.

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