Taurine-induced synaptic potentiation and the late phase of long-term potentiation are related mechanistically

• Published in: Neuropharmacology 2003, Vol.44 (1), p.26-39
• Main Authors: del Olmo, N., Handler, A., Alvarez, L., Bustamante, J., Martín del Río, R., Solís, J.M.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases - metabolism; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; CREB; Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors; Excitatory Postsynaptic Potentials - drug effects; Female; Fiber volley; Fundamental and applied biological sciences. Psychology; Hippocampus - physiology; Hippocampus - ultrastructure; In Vitro Techniques; Long-term potentiation; Long-Term Potentiation - drug effects; Long-Term Potentiation - physiology; Phosphorylation; Protein kinase C; Protein Kinase C - antagonists & inhibitors; Protein synthesis; Rats; Rats, Sprague-Dawley; Receptors, Dopamine D1 - agonists; Receptors, Dopamine D5; Synapses - drug effects; Synapses - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Taurine; Taurine - pharmacology; Taurine - physiology; Vertebrates: nervous system and sense organs
• ISSN: 0028-3908; 1873-7064
• DOI: 10.1016/S0028-3908(02)00310-6

The application of taurine (2-aminoethanesulfonic acid) induces a long-lasting increase of synaptic efficacy and axon excitability (LLP-TAU) in rat hippocampal CA1 area. After taurine withdrawal, LLP-TAU lasted at least 3 h. This fact prompted us to assess whether the mechanisms involved in the maintenance of this particular potentiation were similar to those implicated in the late phase of long-term potentiation (L-LTP). In the presence of KN-62, an inhibitor of calcium/calmodulin-dependent protein kinase, taurine perfusion (10 mM, 30 min) did not affect the induction of LLP-TAU. However, LLP-TAU maintenance was completely suppressed by KT5720, an inhibitor of the cAMP-dependent protein kinase (PKA). Moreover, the late phase of LLP-TAU was blocked by inhibiting protein synthesis with anisomycin. In addition, taurine perfusion increased the phosphorylation of cAMP response element-binding protein (CREB), although did not affect cAMP levels. These features of LLP-TAU do not appear to be caused by the activation of D1/D5 dopamine receptors, as taurine also induced synaptic potentiation in the presence of SCH23390, an antagonist of this type of receptors. Finally, the late phase of both L-LTP and LLP-TAU occluded mutually. These results suggest that taurine triggers the sequence of some of the molecular events involved in the induction of L-LTP.