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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.annemergmed.2005.10.011 Byline: Mauro A.M. Carai (a), Giancarlo Colombo (a), Lawrence S. Quang (b), Timothy J. Maher (c), Gian Luigi Gessa (a) Abstract: Recent reports on fatalities associated with overdoses from 1,4-butanediol (1,4-BD), a precursor of the drug of abuse [gamma]-hydroxybutyric acid (GHB), pose the need for investigations focusing on possible pharmacologic remedies. Accordingly, the present study investigates whether 4-methylpyrazole (4-MP; also termed fomepizole and Antizol), an inhibitor of alcohol dehydrogenase (the enzyme involved in the first step of the conversion of 1,4-BD into GHB), and the [gamma]-aminobutyric acid B (GABA.sub.B) receptor antagonist (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), provides protection against 1,4-BD-induced mortality in CD1 mice. Author Affiliation: (a) Department of Neuroscience, School of Medicine, University of Cagliari, and National Research Council, Institute of Neuroscience, Cagliari, Italy (b) Neuropharmacology and Neurobehavioral Laboratory, Division of Pediatric Pharmacology and Critical Care, Rainbow Babies and Children's Hospital, Cleveland, OH (c) Massachusetts College of Pharmacy and Health Sciences, Boston, MA Article History: Received 18 July 2005; Revised 15 September 2005; Accepted 19 October 2005 Article Note: (footnote) Supervising editor: Stephen R. Thom, MD, PhD, Author contributions: MAMC conceived the study, designed and conducted the experiments, analyzed the data and drafted the manuscript. GC contributed to the conduction of the experiments and manuscript revision. LSQ and TJM contributed to design the experiments and analyze the data; they also revised the manuscript. GLG supervised the conduct of the study and contributed to manuscript revision. MAMC takes responsibility for the paper as a whole., Funding and support: This study was supported in part by the Italian National Research Council (CNR) and by the National Institutes of Health (NIH)/National Institute on Drug Abuse (NIDA) grant #1R03DA14951-02 (LSQ)., Reprints not available from the authors.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.annemergmed.2004.12.013 Byline: Mauro A.M. Carai, Giancarlo Colombo, Gian Luigi Gessa Abstract: In the present study, a number of compounds were tested to evaluate their efficacy in exerting a protective effect on [gamma]-hydroxybutyric acid (GHB)-induced mortality in mice. The drugs investigated were the [gamma]-aminobutyric acid B (GABA.sub.B) receptor antagonist SCH 50911, the GABA.sub.A receptor antagonist bicuculline, the benzodiazepine receptor antagonist flumazenil, the putative GHB receptor antagonist NCS-382, the opioid receptor antagonist naltrexone, and the amino acid and possible neuromodulator, taurine. Author Affiliation: From the Bernard B. Brodie Department of Neuroscience, School of Medicine, University of Cagliari, and CNR Institute of Neuroscience, Section of Cagliari, Italy Article History: Received 18 September 2004; Revised 6 October 2004; Revised 12 November 2004; Revised 7 December 2004; Accepted 15 December 2004 Article Note: (footnote) Author contributions: MAMC conceived the study, designed and conducted the experiments, analyzed the data, and drafted the manuscript. GC contributed to the conducting of the experiments and manuscript revision. GLG obtained research funding, supervised the conduct of the study, and contributed to manuscript revision. MAMC takes responsibility for the paper as a whole. Funding and support: The present study was partially supported by a grant from the Italian Ministry for Education and Research to the 'Center of Excellence on Neurobiology of Dependence,' Department of Neuroscience, University of Cagliari.