Taurine is one of the most abundant free amino acids in the brain and has been identified as an endogenous agonist of both GABA_A and glycine receptors. Although it has been demonstrated that taurine mediates an excitatory action on identified neuronal populations in the developing neocortex, its action on the overall excitability and information processing in neuronal circuits during postnatal development remains elusive. Therefore we recorded visually identified neurons in neocortical slices (400 mm) of mice between the first and fourth postnatal day using whole-cell patch clamp recordings with Cl^--based pipette solutions and investigated the properties of postsynaptic currents (PSCs) induced by focal or bath-application of taurine.

Bath application of taurine significantly increased in a dose dependent manner the frequency of PSCs recorded in pyramidal cells. Since 300 mM taurine was sufficient to induce maximal responses, further experiments were performed with this concentration. In the presence of 0.2 mM TTX taurine-induced PSCs were completely abolished, while a taurine-induced inward current remained in most of neurons. Taurine-induced PSCs were not affected by CNQX (10 mM) or APV (60 mM), demonstrating that AMPA/Kainate and NMDA receptors are not involved in taurine-induced postsynaptic activity. In addition, experiments with low-Cl^- pipette solutions revealed that taurine-induced PSCs reversed at E_GABA, suggesting that they are exclusively mediated via ligand-gated Cl^- channels. The GABA_A antagonist gabazine (3 mM) abolished the taurine-induced PSCs, which can be explained by effects on postsynaptic receptors or on presynaptic cells responding to taurine. A blockade of glycine receptors by 1 mM strychnine induced a reduction in the frequency of taurine-induced PSCs and inward currents, while the PSC amplitude was unaltered. These results indicate that activation of glycine receptors was involved in mediating taurine-induced effects in presynaptic elements of the activated circuits and that the taurine-induced PSCs are mediated mainly by postsynaptic GABA_A receptors. To identify presynaptic neurons responding to taurine, we pressure-applied taurine focally to individual neurons in different regions of the cortical plate far from the recorded neuron. We could identify only few neurons at which focal application of taurine results in synchronized activity at the postsynaptic recorded cell, indicating that only a small fraction of neurons is involved in taurine-induced network activity.

These results demonstrate that taurine activate neuronal networks in the immature neocortex and suggests that this activity is mediated via GABAergic synapses by only a limited subpopulation of neurons in the developing neocortex. Thus taurine may function as an endogenous regulator of excitability in the developing neocortex.