There is no shortage of publications claiming to have detected one or more putative taurine receptors. Results obtained by Kudo et al. [151] on the effects of taurine in the frog spinal cord were interpreted as revealing two taurine receptor subtypes. This conclusion was based on their observation that the application of 10 mM taurine caused a biphasic response consisting of a hyperpolarization followed by a slow onset depolarization. The former was selectively depressed by low concentrations of bicuculline that had no significant effect on the antagonizing action of GABA, whereas the hyperpolarizing component was selectively reduced by a strychnine concentration that had no effect on the response to glycine. Clearly these findings are highly suggestive, but cannot be considered definitive evidence of the presence of taurine-specific receptors. Other studies purporting to have detected taurine receptors in rabbit brain [152] and in RPE cells in culture [153] have been similarly inconclusive. In contrast, the kinetics and pharmacology of a receptor prepared from mammalian brain are consistent with what one might expect of a taurine-specific receptor, i.e., the binding of 3H-taurine was highly specific, and not affected by agonists or antagonists of receptors for glutamate, glycine, benzodiazepine, and GABAB, nor by monovalent or divalent cations [154]. The binding was completely abolished by 0.1 mM cobalt, zinc, or mercury, suggesting the presence of free sulfhydryl groups near or at the ligand-binding site.
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