Effects of d-Cycloserine on Craving to Alcohol Cues in Problem Drinkers: Preliminary Findings

Abstract

Background: It has been shown that the partial N-methyl-d-aspartate (NMDA) agonist d-cycloserine (DCS) facilitates exposure-based learning in humans with anxiety disorders. However, the effects of DCS on exposure to substance cues are still uncertain. Objective: The primary aim of the study was to examine the effects of DCS on exposure sessions to alcohol cues. Methods: Twenty non-treatment-seeking problem drinkers were randomly assigned to receive 50 mg of DCS or placebo 50 minutes prior to each of 3 alcohol cue exposure sessions consisting of 5 exposure trials within an 8-day period. Following this, participants underwent two test sessions without the administration of any medication. The test sessions occurred 3 and 7 days after the last cue exposure session, respectively. Dependent measures included drinking urge and heart rate and drinking urge during the test sessions. Results: Individuals who received DCS showed increased craving to alcohol cues as compared with individuals who received placebo during the first test session. No group difference in drinking urge was found during the second test session. Furthermore, the groups did not differ in heart rate at any of the assessment points. Conclusions: The results suggest that DCS may temporarily augment cue-elicited craving for alcohol. Scientific Significance: As in an earlier study with cocaine-dependent individuals, DCS appears to exhibit a different profile in problem drinkers to those with anxiety disorders. Dose, timing, arousal, and treatment motivation as considerations are discussed, as are methodological considerations and the need for additional studies in this area.

• alcohol
• cue exposure
• cue exposure training
• cue reactivity
• d-cycloserine
• problem drinkers

ACKNOWLEDGMENTS

Dr. Hofmann is a paid consultant by Schering-Plough for research unrelated to this study and he is supported by NIH grant 1R01MH078308. Dr. MacKillop is supported by NIH grants R21AA017696 and K23AA016936; Dr. Hüweler is supported by the Daimler and Benz foundation; and Dr. Kantak is supported by NIH grants 5R01DA011716, 5R01DA024315, and NSF grant OMA0835976. This study was funded by a seed grant from the Boston University Center for Neuroscience.

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.