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

• Published in: Neuropharmacology 2000, Vol.39 (1), p.40-54
• Main Authors: del Olmo, Nuria, Galarreta, Mario, Bustamante, Julián, Martı́n del Rı́o, Rafael, Solı́s, José M
• Format: Article
• Language: English
• Subjects: Animals; Axons - drug effects; Axons - physiology; Biological and medical sciences; Calcium - metabolism; Calcium channels; Calcium Channels, L-Type - physiology; Calcium stores; Calcium-Transporting ATPases - antagonists & inhibitors; Central nervous system; Chelating Agents - pharmacology; Egtazic Acid - analogs & derivatives; Egtazic Acid - pharmacology; Electrophysiology; Excitatory Postsynaptic Potentials - drug effects; Female; Fiber volley; Fundamental and applied biological sciences. Psychology; Hippocampus - physiology; In Vitro Techniques; Kynurenic Acid - pharmacology; Long-term potentiation; Long-Term Potentiation - drug effects; Long-Term Potentiation - physiology; Nifedipine - pharmacology; Rat hippocampal slices; Rats; Rats, Sprague-Dawley; Receptors, Glutamate - physiology; Synapses - drug effects; Synapses - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Taurine; Taurine - pharmacology; Thapsigargin - pharmacology; Vertebrates: nervous system and sense organs
• ISSN: 0028-3908; 1873-7064
• DOI: 10.1016/S0028-3908(99)00078-7

Taurine induces a long-lasting potentiation of excitatory synaptic potentials due to the enhancement of both synaptic efficacy and axon excitability in the CA1 area of rat hippocampal slices. In this study, we characterized the role of Ca 2+ in the generation of these long-lasting taurine effects. Taurine perfusion in a free-Ca 2+ medium did not induce changes in either field excitatory synaptic potentials (fEPSP) slope or fiber volley (FV) amplitude. Intracellular recordings with a micropipette filled with the Ca 2+ chelator BAPTA, prevented the EPSP potentiation induced by taurine in the impaled cell, whereas a long-lasting potentiation of the simultaneously recorded fEPSP was obtained. The depletion of intracellular Ca 2+ stores by thapsigargin (1 μM), an inhibitor of endosomal Ca 2+-ATPase, transformed the taurine-induced potentiation into a transitory process that declined to basal values after taurine withdrawal. Taurine-induced potentiation was not significantly affected by kynurenate (glutamate receptor antagonist), or nifedipine (high-voltage-activated Ca 2+ channel antagonist). But, the presence of nickel (50 μM), an antagonist of low-voltage-activated Ca 2+ channel, inhibited the taurine-induced potentiation, indicating that Ca 2+ influx through this type of Ca 2+ channels could account for the Ca 2+ requirement of the taurine-induced potentiation. Occlusion experiments between tetanus-induced long-term potentiation (LTP) and taurine-induced potentiation indicate that both processes share some common mechanisms during the maintenance period.