Ethanol-like effects of thiopental and ketamine in healthy humans
D. Dickerson, B. Pittman, E. Ralevski, A. Perrino, D. Limoncelli, J. Edgecombe, G. Acampora, JH Krystal, Ismene L. Petrakis
Journal of Psychopharmacology February 1, 2010 DOI: 10.1177/0269881108098612 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 28 |
| Population | Healthy adults aged 21-30 with no personal or family histories of alcoholism |
| Interventions | Thiopental Ketamine |
| Topics | Esketamine Ketamine |
| Key findings | Both thiopental and ketamine produced significant ethanol-like effects and subjective intoxication, but ketamine's effects were more intense and included perceptual alterations not seen with thiopental. The authors propose that GABA-A receptor facilitation contributes to social drinking effects, while NMDA antagonism contributes more to intoxication features. |
Abstract
The γ-aminobutyric acid-A (GABA A ) and N-methyl-D-aspartate (NMDA) receptors mediate aspects of the behavioural effects of alcohol. Prior studies reported drugs that block NMDA receptors or facilitate GABA A receptor function produce ethanol-like effects in humans. The purpose of this study was to compare the ethanol-related effects of two pharmacological agents with known NMDA and GABA A receptor activity. As part of an ongoing, larger study, 28 subjects (age, 21—30) with no personal or family histories of alcoholism were administered subanesthetic doses of the GABA A receptor agonist thiopental, the NMDA receptor antagonist, ketamine and placebo on three separate test days. Various ethanol-related measures were administered. At doses of thiopental and ketamine that produced similar levels of sedation and cognitive effects, both agents produced significant ethanol-like effects and subjective intoxication. However, the intensity of the ethanol-like effects of ketamine was greater than that of thiopental. In addition, ketamine produced alterations in perception that were not produced by thiopental. These data provide further support for a model where GABA A receptor facilitation may contribute significantly to ethanol effects associated with social drinking, whereas NMDA receptor antagonism may contribute to relatively greater extent to features of ethanol ‘intoxication’.