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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on September 20, 2005; DOI: 10.1124/jpet.105.090647

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Received for publication June 7, 2005.
Revised September 14, 2005.
Accepted for publication September 15, 2005.

Volatile Anesthetic Effects on Glutamate versus GABA Release from Isolated Rat Cortical Nerve Terminals: Basal Release

Robert I Westphalen 1 Hugh C Hemmings 1*

1 Weill Cornell Medical College

* Address correspondence to: E-mail: hchemmi{at}med.cornell.edu

Abstract

The effects of three volatile anesthetics (isoflurane, enflurane, and halothane) on basal release of glutamate and GABA from isolated rat cerebrocortical nerve terminals (synaptosomes) were compared using a dual isotope superfusion method. Concentration-dependent effects on basal release differed between anesthetics and transmitters. Over a range of clinical concentrations (0.5-2 times MAC), basal glutamate release was inhibited by all three anesthetics, while basal GABA release was enhanced (isoflurane) or unaffected (enflurane and halothane). These effects may represent a balance of stimulatory and inhibitory mechanisms between transmitters and anesthetics. There were no significant differences between anesthetic effects on basal release in the absence or presence of external Ca2+, while intracellular Ca2+ buffering limited volatile anesthetic inhibition of basal glutamate release. Although these results demonstrate fundamental differences in anesthetic effects on basal release between glutamatergic and GABAergic nerve terminals, all three volatile anesthetics at clinical concentrations consistently reduced the ratio of basal glutamate to GABA release. These actions may contribute to the net depression of glutamatergic excitation and potentiation of GABAergic inhibition characteristic of general anesthesia.


Key words: GABA, basal, glutamate, release, synaptosomes, volatile anesthetics


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