Long-term regulation of N-methyl-D-aspartate receptor subunits and associated synaptic proteins following hippocampal synaptic plasticity
Synaptic plasticity in the dentate gyrus is dependent on activation of the N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors. In this study, we show that synaptic plasticity in turn regulates NMDA receptors, since subunits of the NMDA receptor complex are bidirectionally and independently r...
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| Veröffentlicht in: | Neuroscience 2003-06, Vol.118 (4), p.1003-1013 |
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| creator | WILLIAMS, J. M GUEVREMONT, D KENNARD, J. T. T MASON-PARKER, S. E TATE, W. P ABRAHAM, W. C |
| description | Synaptic plasticity in the dentate gyrus is dependent on activation of the N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors. In this study, we show that synaptic plasticity in turn regulates NMDA receptors, since subunits of the NMDA receptor complex are bidirectionally and independently regulated in the dentate gyrus following activation of perforant synapses in awake animals. Low-frequency stimulation that produced a mild synaptic depression resulted in a decrease in the NMDA receptor subunits NR1 and NR2B 48 h following stimulation. High-frequency stimulation that produced long-term potentiation resulted in an increase in NR1 and NR2B at the same time point. Further investigations revealed that in contrast to NR2B, NR1 levels increased gradually after long-term potentiation induction, reaching a peak level at 48 h, and were insensitive to the competitive NMDA receptor antagonist 3-3(2-carboxypiperazin-4-yl) propyl-1-phosphate. The increased levels of NR1 and NR2B at 48 h were found associated with synaptic membranes and with increased NMDA receptor-associated proteins, postsynaptic density protein 95, neuronal nitric oxide synthase and Ca(2+)/calmodulin-dependent protein kinase II, alpha subunit. These data suggest that the persistence of long-term potentiation is associated with an increase in the number of NMDA receptor complexes, which may be indicative of an increase in synaptic contact area. |
| doi_str_mv | 10.1016/s0306-4522(03)00028-9 |
| format | Article |
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M ; GUEVREMONT, D ; KENNARD, J. T. T ; MASON-PARKER, S. E ; TATE, W. P ; ABRAHAM, W. C</creator><creatorcontrib>WILLIAMS, J. M ; GUEVREMONT, D ; KENNARD, J. T. T ; MASON-PARKER, S. E ; TATE, W. P ; ABRAHAM, W. C</creatorcontrib><description>Synaptic plasticity in the dentate gyrus is dependent on activation of the N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors. In this study, we show that synaptic plasticity in turn regulates NMDA receptors, since subunits of the NMDA receptor complex are bidirectionally and independently regulated in the dentate gyrus following activation of perforant synapses in awake animals. Low-frequency stimulation that produced a mild synaptic depression resulted in a decrease in the NMDA receptor subunits NR1 and NR2B 48 h following stimulation. High-frequency stimulation that produced long-term potentiation resulted in an increase in NR1 and NR2B at the same time point. Further investigations revealed that in contrast to NR2B, NR1 levels increased gradually after long-term potentiation induction, reaching a peak level at 48 h, and were insensitive to the competitive NMDA receptor antagonist 3-3(2-carboxypiperazin-4-yl) propyl-1-phosphate. The increased levels of NR1 and NR2B at 48 h were found associated with synaptic membranes and with increased NMDA receptor-associated proteins, postsynaptic density protein 95, neuronal nitric oxide synthase and Ca(2+)/calmodulin-dependent protein kinase II, alpha subunit. These data suggest that the persistence of long-term potentiation is associated with an increase in the number of NMDA receptor complexes, which may be indicative of an increase in synaptic contact area.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/s0306-4522(03)00028-9</identifier><identifier>PMID: 12732245</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western - methods ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Central nervous system ; Dizocilpine Maleate - pharmacology ; Electric Stimulation - methods ; Electrophysiology ; Electrophysiology - methods ; Excitatory Amino Acid Antagonists - pharmacology ; Excitatory Postsynaptic Potentials - physiology ; Fundamental and applied biological sciences. Psychology ; Hippocampus - anatomy & histology ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - ultrastructure ; In Vitro Techniques ; Long-Term Potentiation - drug effects ; Male ; Microscopy, Electron ; N-Methylaspartate - antagonists & inhibitors ; N-Methylaspartate - pharmacology ; Nerve Tissue Proteins - metabolism ; Neuronal Plasticity - drug effects ; Neuronal Plasticity - physiology ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type I ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate - drug effects ; Receptors, N-Methyl-D-Aspartate - metabolism ; Receptors, N-Methyl-D-Aspartate - ultrastructure ; Synapses - drug effects ; Synapses - metabolism ; Synapses - ultrastructure ; Synaptosomes - metabolism ; Synaptosomes - ultrastructure ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2003-06, Vol.118 (4), p.1003-1013</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-64195c8983853f6f0afbd3a54d87f0f8bf7e14c4a6ba270d303356461f3652843</citedby><cites>FETCH-LOGICAL-c509t-64195c8983853f6f0afbd3a54d87f0f8bf7e14c4a6ba270d303356461f3652843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14762176$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12732245$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WILLIAMS, J. M</creatorcontrib><creatorcontrib>GUEVREMONT, D</creatorcontrib><creatorcontrib>KENNARD, J. T. T</creatorcontrib><creatorcontrib>MASON-PARKER, S. E</creatorcontrib><creatorcontrib>TATE, W. P</creatorcontrib><creatorcontrib>ABRAHAM, W. C</creatorcontrib><title>Long-term regulation of N-methyl-D-aspartate receptor subunits and associated synaptic proteins following hippocampal synaptic plasticity</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Synaptic plasticity in the dentate gyrus is dependent on activation of the N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors. In this study, we show that synaptic plasticity in turn regulates NMDA receptors, since subunits of the NMDA receptor complex are bidirectionally and independently regulated in the dentate gyrus following activation of perforant synapses in awake animals. Low-frequency stimulation that produced a mild synaptic depression resulted in a decrease in the NMDA receptor subunits NR1 and NR2B 48 h following stimulation. High-frequency stimulation that produced long-term potentiation resulted in an increase in NR1 and NR2B at the same time point. Further investigations revealed that in contrast to NR2B, NR1 levels increased gradually after long-term potentiation induction, reaching a peak level at 48 h, and were insensitive to the competitive NMDA receptor antagonist 3-3(2-carboxypiperazin-4-yl) propyl-1-phosphate. The increased levels of NR1 and NR2B at 48 h were found associated with synaptic membranes and with increased NMDA receptor-associated proteins, postsynaptic density protein 95, neuronal nitric oxide synthase and Ca(2+)/calmodulin-dependent protein kinase II, alpha subunit. These data suggest that the persistence of long-term potentiation is associated with an increase in the number of NMDA receptor complexes, which may be indicative of an increase in synaptic contact area.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western - methods</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Central nervous system</subject><subject>Dizocilpine Maleate - pharmacology</subject><subject>Electric Stimulation - methods</subject><subject>Electrophysiology</subject><subject>Electrophysiology - methods</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus - anatomy & histology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - ultrastructure</subject><subject>In Vitro Techniques</subject><subject>Long-Term Potentiation - drug effects</subject><subject>Male</subject><subject>Microscopy, Electron</subject><subject>N-Methylaspartate - antagonists & inhibitors</subject><subject>N-Methylaspartate - pharmacology</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuronal Plasticity - drug effects</subject><subject>Neuronal Plasticity - physiology</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type I</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - ultrastructure</subject><subject>Synapses - drug effects</subject><subject>Synapses - metabolism</subject><subject>Synapses - ultrastructure</subject><subject>Synaptosomes - metabolism</subject><subject>Synaptosomes - ultrastructure</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuO1DAQRS0EYpqBTwB5A4KFwe84SzQ8pRYsgLVVceweIycOtiPUn8Bfk2ZaDDtWtahzq0p1EHrM6EtGmX5VqaCaSMX5cypeUEq5If0dtGOmE6RTUt5Fu7_IBXpQ6_cNokqK--iC8U5wLtUO_drn-UCaLxMu_rAmaDHPOAf8iUy-XR8TeUOgLlAaNL8hzi8tF1zXYZ1jqxjmEUOt2cWtP-J6nGFp0eGl5ObjXHHIKeWfcT7g67gs2cG0QPqHS1C3GtvxIboXIFX_6Fwv0bd3b79efSD7z-8_Xr3eE6do34iWrFfO9EYYJYIOFMIwClByNF2gwQyh80w6CXoA3tFRUCGUlpoFoRU3UlyiZzdztxN_rL42O8XqfEow-7xWu31GC8PZf0Fmes5kd5qobkBXcq3FB7uUOEE5WkbtSZb9cjJhTyYsFfaPLNtvuSfnBesw-fE2dbazAU_PAFQHKRSYXay3nOw0Z50WvwEnmZ-L</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>WILLIAMS, J. M</creator><creator>GUEVREMONT, D</creator><creator>KENNARD, J. T. T</creator><creator>MASON-PARKER, S. E</creator><creator>TATE, W. P</creator><creator>ABRAHAM, W. C</creator><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20030601</creationdate><title>Long-term regulation of N-methyl-D-aspartate receptor subunits and associated synaptic proteins following hippocampal synaptic plasticity</title><author>WILLIAMS, J. M ; GUEVREMONT, D ; KENNARD, J. T. T ; MASON-PARKER, S. E ; TATE, W. P ; ABRAHAM, W. C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-64195c8983853f6f0afbd3a54d87f0f8bf7e14c4a6ba270d303356461f3652843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western - methods</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</topic><topic>Central nervous system</topic><topic>Dizocilpine Maleate - pharmacology</topic><topic>Electric Stimulation - methods</topic><topic>Electrophysiology</topic><topic>Electrophysiology - methods</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - anatomy & histology</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - ultrastructure</topic><topic>In Vitro Techniques</topic><topic>Long-Term Potentiation - drug effects</topic><topic>Male</topic><topic>Microscopy, Electron</topic><topic>N-Methylaspartate - antagonists & inhibitors</topic><topic>N-Methylaspartate - pharmacology</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuronal Plasticity - drug effects</topic><topic>Neuronal Plasticity - physiology</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type I</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - ultrastructure</topic><topic>Synapses - drug effects</topic><topic>Synapses - metabolism</topic><topic>Synapses - ultrastructure</topic><topic>Synaptosomes - metabolism</topic><topic>Synaptosomes - ultrastructure</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WILLIAMS, J. M</creatorcontrib><creatorcontrib>GUEVREMONT, D</creatorcontrib><creatorcontrib>KENNARD, J. T. T</creatorcontrib><creatorcontrib>MASON-PARKER, S. E</creatorcontrib><creatorcontrib>TATE, W. P</creatorcontrib><creatorcontrib>ABRAHAM, W. C</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>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WILLIAMS, J. M</au><au>GUEVREMONT, D</au><au>KENNARD, J. T. T</au><au>MASON-PARKER, S. E</au><au>TATE, W. P</au><au>ABRAHAM, W. C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-term regulation of N-methyl-D-aspartate receptor subunits and associated synaptic proteins following hippocampal synaptic plasticity</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>118</volume><issue>4</issue><spage>1003</spage><epage>1013</epage><pages>1003-1013</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Synaptic plasticity in the dentate gyrus is dependent on activation of the N-methyl-D-aspartate (NMDA)-subtype of glutamate receptors. In this study, we show that synaptic plasticity in turn regulates NMDA receptors, since subunits of the NMDA receptor complex are bidirectionally and independently regulated in the dentate gyrus following activation of perforant synapses in awake animals. Low-frequency stimulation that produced a mild synaptic depression resulted in a decrease in the NMDA receptor subunits NR1 and NR2B 48 h following stimulation. High-frequency stimulation that produced long-term potentiation resulted in an increase in NR1 and NR2B at the same time point. Further investigations revealed that in contrast to NR2B, NR1 levels increased gradually after long-term potentiation induction, reaching a peak level at 48 h, and were insensitive to the competitive NMDA receptor antagonist 3-3(2-carboxypiperazin-4-yl) propyl-1-phosphate. The increased levels of NR1 and NR2B at 48 h were found associated with synaptic membranes and with increased NMDA receptor-associated proteins, postsynaptic density protein 95, neuronal nitric oxide synthase and Ca(2+)/calmodulin-dependent protein kinase II, alpha subunit. These data suggest that the persistence of long-term potentiation is associated with an increase in the number of NMDA receptor complexes, which may be indicative of an increase in synaptic contact area.</abstract><cop>Oxford</cop><pub>Elsevier</pub><pmid>12732245</pmid><doi>10.1016/s0306-4522(03)00028-9</doi><tpages>11</tpages></addata></record> |
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| ispartof | Neuroscience, 2003-06, Vol.118 (4), p.1003-1013 |
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| subjects | Animals Biological and medical sciences Blotting, Western - methods Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - metabolism Central nervous system Dizocilpine Maleate - pharmacology Electric Stimulation - methods Electrophysiology Electrophysiology - methods Excitatory Amino Acid Antagonists - pharmacology Excitatory Postsynaptic Potentials - physiology Fundamental and applied biological sciences. Psychology Hippocampus - anatomy & histology Hippocampus - drug effects Hippocampus - metabolism Hippocampus - ultrastructure In Vitro Techniques Long-Term Potentiation - drug effects Male Microscopy, Electron N-Methylaspartate - antagonists & inhibitors N-Methylaspartate - pharmacology Nerve Tissue Proteins - metabolism Neuronal Plasticity - drug effects Neuronal Plasticity - physiology Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type I Rats Rats, Sprague-Dawley Receptors, N-Methyl-D-Aspartate - drug effects Receptors, N-Methyl-D-Aspartate - metabolism Receptors, N-Methyl-D-Aspartate - ultrastructure Synapses - drug effects Synapses - metabolism Synapses - ultrastructure Synaptosomes - metabolism Synaptosomes - ultrastructure Time Factors Vertebrates: nervous system and sense organs |
| title | Long-term regulation of N-methyl-D-aspartate receptor subunits and associated synaptic proteins following hippocampal synaptic plasticity |
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