dependence, higher [123I]-iomazenil binding to GABA/benzodiazepine receptors was observed in the parietal, frontal, cingulated, temporal, insular, and occipital cortex of non-smoking (but not smoking) ethanol-dependent subjects. Furthermore, the GABA/benzodiazepine receptor availability in the cerebellum and occipital lobe at 1 week of abstinence was correlated with the severity of ethanol withdrawal determined in the subjects every 6 h immediately after admission to the clinic (Staley et al. 2005). Using [11C]-flumazenil PET to measure the pharmacokinetics and pharmacodynamics of midazolam, Lingford-Hughes et al. (2005) showed that ethanol dependence was associated with decreased midazolam-induced time asleep in the absence of reduced benzodiazepine receptor occupancy in ethanol-dependent patients abstinent for at least 6 weeks. The authors hypothesized that this reduced sensitivity in ethanol dependence may reflect a difference in the subunit profile of the GABAA receptors, either as part of the vulnerability to, or as a consequence of their ethanol dependence. More recently, Taylor et al. (2008) found that GABAA receptor function, assayed by midazolam-induced slow saccadic eye movement and sedation, was not affected in ethanol-dependent patients after 2 months of abstinence.
