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Taurine-induced synaptic potentiation and the late phase of long-term potentiation are related mechanistically
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 main...
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Published in: | Neuropharmacology 2003, Vol.44 (1), p.26-39 |
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description | 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. |
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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. 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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.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>CREB</subject><subject>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Female</subject><subject>Fiber volley</subject><subject>Fundamental and applied biological sciences. 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Neuromudulation. Pathways and receptors</topic><topic>CREB</topic><topic>Cyclic AMP-Dependent Protein Kinases - antagonists & inhibitors</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Female</topic><topic>Fiber volley</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - physiology</topic><topic>Hippocampus - ultrastructure</topic><topic>In Vitro Techniques</topic><topic>Long-term potentiation</topic><topic>Long-Term Potentiation - drug effects</topic><topic>Long-Term Potentiation - physiology</topic><topic>Phosphorylation</topic><topic>Protein kinase C</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein synthesis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Dopamine D1 - agonists</topic><topic>Receptors, Dopamine D5</topic><topic>Synapses - drug effects</topic><topic>Synapses - physiology</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Taurine</topic><topic>Taurine - pharmacology</topic><topic>Taurine - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>del Olmo, N.</creatorcontrib><creatorcontrib>Handler, A.</creatorcontrib><creatorcontrib>Alvarez, L.</creatorcontrib><creatorcontrib>Bustamante, J.</creatorcontrib><creatorcontrib>Martín del Río, R.</creatorcontrib><creatorcontrib>Solís, J.M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>del Olmo, N.</au><au>Handler, A.</au><au>Alvarez, L.</au><au>Bustamante, J.</au><au>Martín del Río, R.</au><au>Solís, J.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Taurine-induced synaptic potentiation and the late phase of long-term potentiation are related mechanistically</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2003</date><risdate>2003</risdate><volume>44</volume><issue>1</issue><spage>26</spage><epage>39</epage><pages>26-39</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>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.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12559119</pmid><doi>10.1016/S0028-3908(02)00310-6</doi><tpages>14</tpages></addata></record> |
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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 |
title | Taurine-induced synaptic potentiation and the late phase of long-term potentiation are related mechanistically |
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