Taurine-induced synaptic potentiation: role of calcium and interaction with LTP

Taurine induces a long-lasting potentiation of excitatory synaptic potentia ls due to the enhancement of both synaptic efficacy and axon excitability i n the CAI area of rat hippocampal slices. In this study we characterized th e role of Ca2+ in the generation of these long-lasting taurine effects. Tau rine perfusion in a free-Ca2+ medium did not induce changes in either field excitatory synaptic potentials (fEPSP) slope or fiber volley (FV) amplitud e. Intracellular recordings with a micropipette filled with the Ca2+ chelat or BAPTA prevented the EPSP potentiation induced by taurine in the impaled cell, whereas a long-lasting potentiation of the simultaneously recorded fE PSP was obtained. The depletion of intracellular Ca2+ stores by thapsigargi n (1 mu M), an inhibitor of endosomal Ca2+ -ATPase, transformed the taurine -induced potentiation into a transitory process that declined to basal valu es after taurine withdrawal. Taurine-induced potentiation was not significa ntly affected by kynurenate (glutamate receptor antagonist), or nifedipine (high-voltage-activated Ca2+ channel antagonist). But, the presence of nick el (50 mu M), an antagonist of low-voltage-activated Ca2+ channel, inhibite d the taurine-induced potentiation, indicating that Ca2+ influx through thi s type of Ca2+ channels could account for the Ca2+ requirement of the tauri ne-induced potentiation. Occlusion experiments between tetanus-induced long -term potentiation (LTP) and taurine-induced potentiation indicate that bot h processes share some common mechanisms during the maintenance period. (C) 1999 Elsevier Science Ltd. All rights reserved.