© Neuroscience-Net Volume 1, Article #10004

Received June 2, 1996 Accepted for Publication July 2, 1996 Published July 15, 1996

Tina K. Machu, Dept. of Pharmacology Texas Tech University Health Sciences Center

Send correspondence to:

Tina K. Machu, Ph.D.
Dept. of Pharmacology
Texas Tech University Health Sciences Center
3601 Fourth Street
Lubbock, TX 79430
806-743-2425
FAX 806-743-2744
E-mail: phrtkm@ttuhsc.edu

KEY WORDS: receptor, ethanol, alcohol, anesthetic, halothane, oocyte,

ABSTRACT
(Neuroscience-Net, Volume 1, Article #10004; July 15, 1996)

The glycine receptor is a member of the superfamily of ligand-gated ion channels, of which many are important targets for alcohol and anesthetic actions. In the present study, I examined the sensitivity of cloned alpha1 and alpha2 homomeric glycine receptors expressed in Xenopus oocytes to ethanol, butanol, and halothane. Ethanol (50-200 mM) significantly potentiated responses seen with low (<EC20) glycine concentrations in both alpha1 and alpha2 subunit containing oocytes. Butanol (2.5-40 mM) potentiated glycine receptor function to a similar degree in oocytes expressing alpha1 or alpha2 subunits. Enhancement of glycine responses by butanol ranged from ~ 20 to1000%. The volatile anesthetic, halothane, increased glycine mediated currents in oocytes expressing either subunit. Increases of approximately 40 to 500% were observed with concentrations of halothane ranging from 0.16 to 10 mM. Significant increases in glycine receptor function were observed below 1 minimum alveolar concentration for anesthesia (MAC). The ability of both alcohols and halothane to enhance receptor function declined as glycine concentrations were increased, suggesting that these drugs enhance the potency and not the efficacy of the receptor. Since glycine receptor subtypes are sensitive to pharmacologically relevant concentrations of alcohols and anesthetics, they are good candidates for participating in the mechanism(s) of action of these drugs. © 1996 Neuroscience-Net.