The physiological role of taurine, one of the most abundant free amino acids in the mammalian brain, is still poorly understood. We have found that bath application of the amino acid taurine induces two opposite actions on field excitatory synaptic potentials (fEPSP) recorded in the CA1 area of hippocampal slices: a decrease in fEPSP slope prevented by GABAA antagonists, and a long-lasting potentiation of fEPSP independent of GABAA or NMDA receptor activation. Two long-lasting processes account for this taurine-induced potentiation: (1) an increase in synaptic efficacy that is accompanied neither by modifications in the basic postsynaptic membrane electrical properties nor by those presynaptic changes involved in fEPSP paired-pulse facilitation; and (2) an increase in the axon excitability revealed by a reduction on the threshold for antidromic action potential activation. In addition, taurine perfusion also induces a long-lasting increase in intracellularly recorded EPSPs and monosynaptically activated IPSPs. A number of experimental observations such as temperature dependence, extracellular Na+ concentration dependence, and saturation studies, although they are not unequivocally conclusive, suggest that the taurine uptake system is required for the taurine-induced fEPSP potentiation. Our data describe a new taurine action defined as a potentiation of synaptic transmission due in part to an increment in presynaptic axon excitability and in synaptic efficacy.