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BJA Advance Access originally published online on February 17, 2009
British Journal of Anaesthesia 2009 102(4):515-522; doi:10.1093/bja/aep009
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© The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournal.org

Loss of surface N-methyl-D-aspartate receptor proteins in mouse cortical neurones during anaesthesia induced by chloral hydrate in vivo

A. LacKamp1, G.-C. Zhang2, L.-M. Mao2, E. E. Fibuch1 and J. Q. Wang1,2,*

1 Department of Anesthesiology
2 Department of Basic Medical Science, University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA

* Corresponding author. E-mail: wangjq{at}umkc.edu

Background: Anaesthetics may target ionotropic glutamate receptors in brain cells to produce their biological actions. Membrane-bound ionotropic glutamate receptors undergo dynamic trafficking between the surface membrane and intracellular organelles. Their subcellular distribution is subject to modulation by changing synaptic inputs and determines the efficacy and strength of excitatory synapses. It has not been explored whether anaesthesia has any impact on surface glutamate receptor expression. In this study, the effect of general anaesthesia on expression of N-methyl-D-aspartate (NMDA) receptors in the surface and intracellular pools of cortical neurones was investigated in vivo.

Methods: General anaesthesia was induced by intraperitoneal injection of chloral hydrate in adult male mice. Surface protein cross-linking assays were performed to detect changes in distribution of NMDA receptor subunits (NR1, NR2A, and NR2B) in the surface and intracellular compartments of cerebral cortical neurones.

Results: Chloral hydrate did not alter the total amounts of NR1, NR2A, and NR2B proteins in cortical neurones. However, the drug reduced NR1 proteins in the surface pool of these neurones, and induced a proportional increase in NR1 in the intracellular pool. Similar redistribution of NR2B subunits was observed between the two distinct pools. The changes in NR1 and NR2B were rapid and remained throughout the duration of anaesthesia. NR2A proteins were not altered in the surface or intracellular pool in response to chloral hydrate.

Conclusions: These data demonstrate that subcellular expression of NR1 and NR2B in cortical neurones is sensitive to anaesthesia. Chloral hydrate reduces surface-expressed NMDA receptors (specifically NR2B-containing NMDA receptors) in these neurones in vivo.

Keywords: anaesthetics; cerebral cortex; glutamate receptor; NR1; NR2A; NR2B


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