Abstract

The recognition of taurine and GABA, two neuroactive amino acids, as normal constituents of nervous tissue, occurred almost at the same time (1,43). Their structural similarity and the resemblance of their effects on neuronal activity had suggested similar roles for them in nervous function. However, whereas during the last few years an impressive amount of evidence has accumulated supporting a role for GABA as an inhibitory neurotransmitter (44), the elucidation of the role of taurine in nervous function has been particularly difficult. Some experimental evidence exists supporting a role for taurine as a neurotransmitter. It has been demonstrated that taurine, when applied via microiontophoresis, excerts a depressant effect on neuronal activity in several regions of the central nervous system (10–12). However, the unsuccessful search for specific blockers of this action of taurine, together with the antagonism shown by strychnine and bicuculline on inhibitory effects of taurine (10–12), have raised some doubts about the specificity of taurine as an inhibitory neurotransmitter itself. Since strychnine and bicuculline are likely to be specific antagonists of GABA and glycine receptors, the effect of taurine on post-synaptic neurons blocked by these drugs could be mediated through an interaction with GABA and glycine receptors. Studies in vitro using biochemical techniques to characterize GABA and glycine postsynaptic receptors in several regions of the CNS, have clearly shown a significant interaction of taurine with GABA and glycine binding to their specific receptors (15,51). Furthermore, the identification of taurine receptors by this technique, has proved unsuccessful (Lopez-Colome, this volume).

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