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Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels.
Abstract
The interaction of ethanol with gamma-aminobutyric acid (GABA)-mediated 36-Cl-influx and its modulation by various drugs was investigated in C57 mice spinal cord cultured neurons. Ethanol (5-100 mM) potentiated the effect of GABA on 36Cl-influx; whereas at concentrations greater than or equal to 50 mM ethanol activated Cl- channels directly. The effect of ethanol was specific for GABAA receptor-gated Cl- channels, as ethanol did not potentiate glycine-induced 36Cl-influx in the same neurons. Both the enhancing and direct effects of ethanol on 36Cl-influx were blocked by GABA antagonists like bicuculline, picrotoxinin and inverse agonists of the benzodiazepine site like the imidazodiazepine R015-4513 (ethyl-8-azido-5,6-dihydro-5-methyl-6-oxo-4H-imidazo [1,5 alpha], [1,4]benzodiazepine-3-carboxylate) and N-methyl-beta-carboline-3-carboxamide (FG-7142). Ethanol potentiating effect of GABA-induced 36Cl-influx was also reversed by methyl-6,7-dimethyl-4-ethyl-beta-carboline-3-carboxylate. The effects of the inverse agonists were blocked by the benzodiazepine receptor antagonist R015-1788. Both R015-4513 and FG-7142 reversed direct and GABA potentiating effects of ethanol effect at concentrations lower than those that exhibit inverse agonistic activity in the 36Cl-influx assay in cultured neurons. These results suggest that ethanol facilitation of GABAAergic transmission involves GABA receptor-gated Cl- channels and that this interaction may be responsible for some of the pharmacological effects of ethanol.
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Citations
Cited by
Ethanol Inhibits NMDA-Activated Ion Current in Hippocampal Neurons
Lovinger, D. M., White, G., & Weight, F. F. (1989) · Science · doi:10.1126/science.2467382 · Cited by 1,448
Effects of Moderate Alcohol Consumption on the Central Nervous System*
Eckardt, M. J., File, S. E., Gessa, G. L., Grant, K. A., Guerri, C., Hoffman, P. L., Kalant, H., Koob, G. F., Li, T., & Tabakoff, B. (1998) · Alcoholism: Clinical and Experimental Research · doi:10.1111/j.1530-0277.1998.tb03695.x · Cited by 622
Wallner, M., Hanchar, H. J., & Olsen, R. W. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2435171100 · Cited by 462
Cagetti, E., Liang, J., Spigelman, I., & Olsen, R. W. (2003) · Molecular Pharmacology · doi:10.1124/mol.63.1.53 · Cited by 320
GABAA receptor antagonism in the extended amygdala decreases ethanol self-administration in rats
Hyytiä, P., & Koob, G. F. (1995) · European Journal of Pharmacology · doi:10.1016/0014-2999(95)00314-b · Cited by 302
Metadata
- Authors
- Mehta, A. K., & Ticku, M. K.
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 1988-08
- Volume
- 246
- Issue
- 2
- Pages
- 558-564
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W2162925069
- Cited by
- 282
- References
- 0
- FWCI
- 6.95
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels. https://app.cochat.ai/papers/10.1016/s0022-3565(25)22106-1
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- Mehta, A. K., & Ticku, M. K. (1988). Ethanol potentiation of GABAergic transmission in cultured spinal cord neurons involves gamma-aminobutyric acidA-gated chloride channels. The Journal of Pharmacology and Experimental Therapeutics. https://doi.org/10.1016/s0022-3565(25)22106-1
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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