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Research ArticleNEUROPHARMACOLOGY

Ethanol Potentiation of Glycine-Induced Responses in Dissociated Neurons of Rat Ventral Tegmental Area

Jiang Hong Ye, Liang Tao, Jun Ren, Rebecca Schaefer, Kresimir Krnjević, Philip L. Liu, Dolores A. Schiller and Joseph J. McArdle
Journal of Pharmacology and Experimental Therapeutics January 2001, 296 (1) 77-83;
Jiang Hong Ye
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Liang Tao
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Jun Ren
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Rebecca Schaefer
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Kresimir Krnjević
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Philip L. Liu
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Dolores A. Schiller
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Joseph J. McArdle
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Abstract

The potentiation of glycine-induced responses by ethanol (EtOH) was studied in neurons freshly dissociated from the ventral tegmental area (VTA) of 5- to 14-day-old postnatal rats using whole-cell and gramicidin-perforated patch-clamp techniques. Under current-clamp conditions, EtOH increased glycine-induced membrane depolarization and action potential firing. Under voltage-clamp conditions, EtOH (0.1–40 mM) alone did not elicit a current. When coapplied with glycine, EtOH enhanced the glycine-induced current in 35% (180 of 474) of the neurons. The EtOH-induced enhancement of glycine current was independent of membrane potential (between −60 and +60 mV); the reversal potential was not changed. Concentration-response analysis showed that in the presence of EtOH (10 mM), the EC50 for glycine decreased from 25 ± 4 to 14 ± 3 μM; the Hill coefficient increased from 1.5 ± 0.2 to 1.9 ± 0.3. Kinetic analysis of glycine currents indicated that EtOH decreased the time constant of activation and increased the time constant of deactivation of glycine-gated chloride channels. EtOH may accelerate glycine association with its receptor at the agonist binding site and increase the apparent agonist affinity. Our observations suggest that, at pharmacologically relevant concentrations, EtOH alters the function of glycine receptors and thus the excitability of neonatal VTA neurons. This action of EtOH may contribute to the neurobehavioral disturbances associated with fetal alcohol syndrome.

Footnotes

  • Send reprint requests to: Jiang Hong Ye, Department of Anesthesiology, New Jersey Medical School (UMDNJ), 185 South Orange Ave., Newark, NJ 07103-2714. E-mail: ye{at}umdnj.edu

  • This study was supported by National Institute of Alcohol Abuse and Alcoholism, National Institute of Health Grant AA-11989 (to J.H.Y.).

  • Abbreviations:
    CNS
    central nervous system
    EtOH
    ethanol
    GABA
    γ-aminobutyric acid
    GlyR
    glycine receptor/channel
    STR
    strychnine
    IGly
    glycine-activated current
    VTA
    ventral tegmental area
    VH
    holding potential
    EGly
    reversal potential of glycine current
    τd
    time constant of decay
    τon
    activation time constant
    τoff
    deactivation time constant
    • Received August 1, 2000.
    • Accepted September 15, 2000.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 296 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 296, Issue 1
1 Jan 2001
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Research ArticleNEUROPHARMACOLOGY

Ethanol Potentiation of Glycine-Induced Responses in Dissociated Neurons of Rat Ventral Tegmental Area

Jiang Hong Ye, Liang Tao, Jun Ren, Rebecca Schaefer, Kresimir Krnjević, Philip L. Liu, Dolores A. Schiller and Joseph J. McArdle
Journal of Pharmacology and Experimental Therapeutics January 1, 2001, 296 (1) 77-83;

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Research ArticleNEUROPHARMACOLOGY

Ethanol Potentiation of Glycine-Induced Responses in Dissociated Neurons of Rat Ventral Tegmental Area

Jiang Hong Ye, Liang Tao, Jun Ren, Rebecca Schaefer, Kresimir Krnjević, Philip L. Liu, Dolores A. Schiller and Joseph J. McArdle
Journal of Pharmacology and Experimental Therapeutics January 1, 2001, 296 (1) 77-83;
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