Abstract

Since 19791 it has been recognised that taurine, together with some of its precursors, e.g. cysteic acid, and major metabolic products, e.g. taurocholic acid, is able to alter some of ethanol-elicited responses; taurocholic acid decreases ethanol preference, while cysteic acid diminishes circulating ethanol concentrations. Homotaurine, which is formed by the addition of a methyl group to taurine, Figure 1, has also been identified as an agonist of GABA receptors2 and will reduce ethanol consumption in spontaneously drinking rats. Further chemical modification of this compound by the addition of an acetyl group, and then calcium bridging of two N-acetyl homotaurine dimers results in the formation of calcium acetyl homotaurine (Fig. 1) which has also been demonstrated to significantly reduces voluntary intake of ethanol, an effect which was inhibited when the GABAA receptors were blocked by the

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