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Cerebral Cortex Advance Access originally published online on January 12, 2005
Cerebral Cortex 2005 15(9):1322-1331; doi:10.1093/cercor/bhi015
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© Oxford University Press 2005; all rights reserved

Anesthetic-induced Burst Suppression EEG Activity Requires Glutamate-mediated Excitatory Synaptic Transmission

Heath S. Lukatch1, Cynthia E. Kiddoo2 and M. Bruce MacIver1,3

1 Stanford Neuroscience Program and Neuropharmacology Laboratory, Stanford University School of Medicine, Stanford, CA 94305–5117, USA, 2 Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139-4307, USA, and 3 Department of Anesthesia, Stanford University School of Medicine, Stanford, CA 94305-5117, USA

Address correspondence to: Dr M. Bruce MacIver, SUMC S 288 MC 5117, Department of Anesthesia, Stanford, CA 94305-5117, USA. Email: maciver{at}stanford.edu.

Many anesthetics evoke electroencephalogram (EEG) burst suppression activity in humans and animals during anesthesia, and the mechanisms underlying this activity remain unclear. The present study used a rat neocortical brain slice EEG preparation to investigate excitatory synaptic mechanisms underlying anesthetic-induced burst suppression activity. Excitatory synaptic mechanisms associated with burst suppression activity were probed using glutamate receptor antagonists (CNQX and APV), GABA receptor antagonists, and simultaneous whole cell patch clamp and microelectrode EEG recordings. Clinically relevant concentrations of thiopental (50–70 µM), propofol (5–10 µM) or isoflurane (0.7–2.1 vol%, 0.5–1.5 rat minimum aveolar concentration (MAC), 200–700 µM) evoked delta slow wave activity and burst suppression EEG patterns similar to in vivo responses. These effects on EEG signals were blocked by glutamate receptor antagonists CNQX (8.6 µM) or APV (50 µM). Depolarizing intracellular bursts (amplitude = 34.7 ± 4.5 mV; half width = 132 ± 60 ms) always accompanied EEG bursts, and hyperpolarization increased intracellular burst amplitudes. Barrages of glutamate-mediated excitatory events initiated EEG bursting activity. Glutamate-mediated excitatory postsynaptic currents were significantly depressed by higher anesthetic concentrations that depressed burst suppression EEG activity. A GABAA agonist produced a similar EEG effect to the anesthetics. It appears that anesthetic effects at both glutamate and GABA synapses contribute to EEG patterns seen during anesthesia.

Key Words: EPSP • IPSC • membrane • neocortex • synapse • voltage clamp


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