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We are particularly pleased that Alcohol and Alcoholism has dedicated this special collection to ‘Sex and Gender differences in Alcohol Use Disorder’. To date, a series of preclinical and clinical studies have tried to shed light on the similarities and differences in the field of alcohol research between men and women (Agabio et al., 2016a and 2017; Salvatore et al., 2017; McHugh et al., 2018; Ait-Daoud et al., 2019; Becker and Chartoff, 2019). However, our understanding of the complexities on this topic remains limited.

Aims: (i) To evaluate the prevalence of alcohol use disorders, and at risk-drinking among outpatients admitted to the Division of Psychiatry, University of Cagliari, Italy, for mood disorders, and (ii) to compare the sensitivity and specificity of the questionnaires used. Methods: Fifty-six patients affected by mood disorders answered to the questions of (i) The NIAAA Guide for identification of at-risk drinking, (ii) AUDIT questionnaire, (iii) The CAGE questionnaire and, (iv) SCID-I application forms for mood and alcohol use disorders. Results: Fourteen subjects (25%) met the criteria for alcohol use disorders according to SCID-I; 17 (30.4%) achieved a score ≥ 1 in CAGE questionnaire; 12 (21.4%) reached AUDIT scores of ≥8 and 4 for men and women, respectively; 12 (21.4%) provided positive answers to NIAAA Guide. Despite these prevalence rates, no diagnosis of alcohol use disorders had previously been registered in their medical records. The CAGE questionnaire achieved the highest values of sensitivity and specificity in detecting alcohol use disorders tested against that of the SCID-I. Conclusions: Alcohol use disorders and at-risk drinking are frequent in patients affected by mood disorders, although often underestimated; this underestimation was virtually absolute in the sample of patients investigated. Combination of the CAGE questionnaire plus the first questions in the NIAAA Guide may be an effective tool for use in the identification of psychiatric patients with possible alcohol use disorders or at-risk drinking.

Experiment 1 in the present study investigated the time course and dose range of gamma-hydroxybutyric acid (GHB) to reduce voluntary ethanol intake in selectively bred Sardinian ethanol-preferring (sP) rats. Ethanol (10%, v/v) and tap water were offered under the two-bottle free choice regimen with unlimited access. GHB (200, 300, and 400 mg/kg, i.p.) was administered 15 20 min prior to the start of the dark phase of the light-dark cycle. Ethanol and water intakes were recorded at different time intervals during the dark phase. GHB significantly reduced ethanol intake at doses of 300 and 400 mg/kg; statistical significance occurred only at the 15-min and 30-min observation times. The GHB dose of 300 mg/kg was devoid of any sedative effect, as demonstrated in Experiment 2 by the lack of any impairment of spontaneous locomotor activity. Finally, this dose of GHB was also found to exert a robust anxiolytic effect in sP rats tested on the elevated plus maze (Experiment 3). Collectively, the results of the present study demonstrate that a non-sedative and anxiolytic dose of GHB effectively reduced voluntary ethanol intake in sP rats. The rapid onset of the reducing effect of GHB on ethanol intake, as well as its anxiolytic effect, are discussed in terms of adding further support to the hypothesis that GHB may control alcohol craving and consumption in humans by substituting for ethanol's reinforcing effects.

The present study was designed to assess the temporal pattern of ethanol intake over a 24 h period in selectively bred, Sardinian alcohol-preferring (sP) rats. Ethanol intake occurred under the two-bottle, free choice regimen. sP rats consumed ethanol in three distinct peaks, rather regularly distributed over the 12 h dark phase of the light-dark cycle and positively correlated with food intake episodes. The temporal distribution of ethanol intake and estimated blood alcohol levels are consistent with the hypothesis that sP rats voluntarily drink ethanol for its pharmacological effects.

( Received 28 August 2004; first review notified 12 September 2004; in revised form 28 September 2004; accepted 7 October 2004 ) Thiamine (vitamin B1) is a water-soluble vitamin that is involved in the metabolism of glucose and lipids as well as in the production of glucose-derived neurotransmitters (see Cook et al ., 1998). Its deficiency leads to a variety of neurological and cardiovascular symptoms and signs. Early symptoms may include fatigue, weakness and emotional disturbance, whereas prolonged gradual deficiency may lead to a form of polyneuritis (known as dry beriberi), cardiac failure or peripheral oedema (wet beriberi) (Thomson, 2000). Severe thiamine deficiency (TD) may result in the development of Wernicke's encephalopathy (WE). The classical signs of WE are ocular motility disorders (nystagmus, ophthalmoplegia), ataxia and mental changes (confusion, drowsiness, obtundation, clouding of consciousness, pre-coma and coma), although minor episodes of 'subclinical' encephalopathies are frequent (Reuler et al ., 1985). An appropriate treatment may correct most of these abnormalities; in contrast, the lack of a diagnosis of WE may result in serious consequences (Reuler et al ., 1985 …