In vivo neuroimaging studies have shown that 1–6 months abstinent male ethanol-dependent subjects have reduced binding of tracers for the GABA/benzodiazepine receptor in the frontal cortex, measured by [11C]-flumazenil positron emission tomography (PET, Gilman et al. 1996) or [123I]-iomazenil single photon emission computed tomography (SPECT, Abi-Dargham et al. 1998; Lingford-Hughes et al. 1998). A trend for a reduced [123I]-iomazenil binding was reported in ethanol-dependent women withdrawn from ethanol with benzodiazepines and abstinent from ethanol for at least 3 months (Lingford-Hughes et al. 2000). Using a [2-deoxy-2[18F]-fluoro-D-glucose] PET study, Volkow et al. (1997) found that the inhibitory response to a lorazepam challenge was blunted in the orbitofrontal cortex and cingulate gyrus in 8–11 weeks (during detoxification) abstinent ethanol-dependent subjects, suggesting reduced GABA/benzodiazepine receptor function. However, this study did not report withdrawal intensity. In contrast, after 1 week of abstinence from ethanol 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
