Taurine abnormality may underlie developmental disorders via perturbation of multimodal GABA actions

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In immature neurons, intracellular Cl- concentration is high due to balance of Cl- transporters, promoting depolarizing GABA action by efflux of Cl- along with its electrical gradient. These GABAA receptor-mediated actions are excitatory and/or non-synaptic tonic depolarization in immature brain. These GABAA receptor activation are necessary for neurogenesis, differentiation, migration, and synaptogenesis of developing brain. Therfore, perturbation of the multimodal GABA actions may underlie fetal and neonatal brain disorders. By hypothesizing fetal taurine of maternal origin as an endogenous agonist of fetal GABAA receptor, we have studied how taurine interact with development and pathogenesis of fetal cortex.