A Critical Interaction between NR2B and MAGUK in L-DOPA Induced Dyskinesia
Abnormal function of NMDA receptor has been suggested to be correlated with the pathogenesis of Parkinson's disease (PD) as well as with the development of l-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. Here we show that NMDA receptor NR2 subunits display specific alterations of thei...
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| creator | Gardoni, Fabrizio Picconi, Barbara Ghiglieri, Veronica Polli, Federica Bagetta, Vincenza Bernardi, Giorgio Cattabeni, Flaminio Di Luca, Monica Calabresi, Paolo |
| description | Abnormal function of NMDA receptor has been suggested to be correlated with the pathogenesis of Parkinson's disease (PD) as well as with the development of l-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. Here we show that NMDA receptor NR2 subunits display specific alterations of their subcellular distribution in striata from unilateral 6-hydroxydopamine-lesioned, L-DOPA-treated dyskinetic, and L-DOPA-treated nondyskinetic rats. Dyskinetic animals have significantly higher levels of NR2A subunit in the postsynaptic compartment than all other experimental groups, whereas NR2B subunit shows a significant reduction in both dopamine-denervated and dyskinetic rats. These events are paralleled by profound modifications of NMDA receptor NR2B subunit association with interacting elements, i.e., members of the membrane-associated guanylate kinase (MAGUK) protein family postsynaptic density-95, synapse-associated protein-97 and synapse-associated protein-102. Treatment of nondyskinetic animals with a synthetic peptide (TAT2B) able to affect NR2B binding to MAGUK proteins as well as synaptic localization of this subunit in nondyskinetic rats was sufficient to induce a shift of treated rats toward a dyskinetic motor behavior. These data indicate abnormal NR2B redistribution between synaptic and extrasynaptic membranes as an important molecular disturbance of the glutamatergic synapse involved in L-DOPA-induced dyskinesia. |
| doi_str_mv | 10.1523/JNEUROSCI.5326-05.2006 |
| format | Article |
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Here we show that NMDA receptor NR2 subunits display specific alterations of their subcellular distribution in striata from unilateral 6-hydroxydopamine-lesioned, L-DOPA-treated dyskinetic, and L-DOPA-treated nondyskinetic rats. Dyskinetic animals have significantly higher levels of NR2A subunit in the postsynaptic compartment than all other experimental groups, whereas NR2B subunit shows a significant reduction in both dopamine-denervated and dyskinetic rats. These events are paralleled by profound modifications of NMDA receptor NR2B subunit association with interacting elements, i.e., members of the membrane-associated guanylate kinase (MAGUK) protein family postsynaptic density-95, synapse-associated protein-97 and synapse-associated protein-102. Treatment of nondyskinetic animals with a synthetic peptide (TAT2B) able to affect NR2B binding to MAGUK proteins as well as synaptic localization of this subunit in nondyskinetic rats was sufficient to induce a shift of treated rats toward a dyskinetic motor behavior. These data indicate abnormal NR2B redistribution between synaptic and extrasynaptic membranes as an important molecular disturbance of the glutamatergic synapse involved in L-DOPA-induced dyskinesia.</description><identifier>ISSN: 0270-6474</identifier><identifier>EISSN: 1529-2401</identifier><identifier>DOI: 10.1523/JNEUROSCI.5326-05.2006</identifier><identifier>PMID: 16540568</identifier><language>eng</language><publisher>United States: Soc Neuroscience</publisher><subject>Adaptor Proteins, Signal Transducing - chemistry ; Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Antiparkinson Agents - therapeutic use ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases - metabolism ; Corpus Striatum - chemistry ; Corpus Striatum - ultrastructure ; Disks Large Homolog 4 Protein ; Intracellular Signaling Peptides and Proteins - chemistry ; Intracellular Signaling Peptides and Proteins - metabolism ; Levodopa - therapeutic use ; Male ; Membrane Proteins - chemistry ; Membrane Proteins - metabolism ; Motor Activity - drug effects ; Neuropeptides - chemistry ; Neuropeptides - metabolism ; Oxidopamine - toxicity ; Parkinsonian Disorders - chemically induced ; Parkinsonian Disorders - drug therapy ; Parkinsonian Disorders - metabolism ; Parkinsonian Disorders - pathology ; Phosphorylation ; Protein Binding ; Protein Interaction Mapping ; Protein Processing, Post-Translational ; Protein Structure, Tertiary ; Protein Transport ; Protein-Tyrosine Kinases - metabolism ; Psychomotor Performance - drug effects ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate - analysis ; Receptors, N-Methyl-D-Aspartate - chemistry ; Receptors, N-Methyl-D-Aspartate - metabolism ; Recombinant Fusion Proteins - pharmacology ; Recombinant Fusion Proteins - therapeutic use ; Subcellular Fractions - chemistry ; Synapses - chemistry</subject><ispartof>The Journal of neuroscience, 2006-03, Vol.26 (11), p.2914-2922</ispartof><rights>Copyright © 2006 Society for Neuroscience 0270-6474/06/262914-09$15.00/0 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c594t-395d188ab4ea540560d112d06ea9eb240a54a0986e43c51baf78296123df29503</citedby><cites>FETCH-LOGICAL-c594t-395d188ab4ea540560d112d06ea9eb240a54a0986e43c51baf78296123df29503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6673976/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6673976/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16540568$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gardoni, Fabrizio</creatorcontrib><creatorcontrib>Picconi, Barbara</creatorcontrib><creatorcontrib>Ghiglieri, Veronica</creatorcontrib><creatorcontrib>Polli, Federica</creatorcontrib><creatorcontrib>Bagetta, Vincenza</creatorcontrib><creatorcontrib>Bernardi, Giorgio</creatorcontrib><creatorcontrib>Cattabeni, Flaminio</creatorcontrib><creatorcontrib>Di Luca, Monica</creatorcontrib><creatorcontrib>Calabresi, Paolo</creatorcontrib><title>A Critical Interaction between NR2B and MAGUK in L-DOPA Induced Dyskinesia</title><title>The Journal of neuroscience</title><addtitle>J Neurosci</addtitle><description>Abnormal function of NMDA receptor has been suggested to be correlated with the pathogenesis of Parkinson's disease (PD) as well as with the development of l-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. Here we show that NMDA receptor NR2 subunits display specific alterations of their subcellular distribution in striata from unilateral 6-hydroxydopamine-lesioned, L-DOPA-treated dyskinetic, and L-DOPA-treated nondyskinetic rats. Dyskinetic animals have significantly higher levels of NR2A subunit in the postsynaptic compartment than all other experimental groups, whereas NR2B subunit shows a significant reduction in both dopamine-denervated and dyskinetic rats. These events are paralleled by profound modifications of NMDA receptor NR2B subunit association with interacting elements, i.e., members of the membrane-associated guanylate kinase (MAGUK) protein family postsynaptic density-95, synapse-associated protein-97 and synapse-associated protein-102. Treatment of nondyskinetic animals with a synthetic peptide (TAT2B) able to affect NR2B binding to MAGUK proteins as well as synaptic localization of this subunit in nondyskinetic rats was sufficient to induce a shift of treated rats toward a dyskinetic motor behavior. These data indicate abnormal NR2B redistribution between synaptic and extrasynaptic membranes as an important molecular disturbance of the glutamatergic synapse involved in L-DOPA-induced dyskinesia.</description><subject>Adaptor Proteins, Signal Transducing - chemistry</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Antiparkinson Agents - therapeutic use</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2</subject><subject>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</subject><subject>Corpus Striatum - chemistry</subject><subject>Corpus Striatum - ultrastructure</subject><subject>Disks Large Homolog 4 Protein</subject><subject>Intracellular Signaling Peptides and Proteins - chemistry</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Levodopa - therapeutic use</subject><subject>Male</subject><subject>Membrane Proteins - chemistry</subject><subject>Membrane Proteins - metabolism</subject><subject>Motor Activity - drug effects</subject><subject>Neuropeptides - chemistry</subject><subject>Neuropeptides - metabolism</subject><subject>Oxidopamine - toxicity</subject><subject>Parkinsonian Disorders - chemically induced</subject><subject>Parkinsonian Disorders - drug therapy</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Parkinsonian Disorders - pathology</subject><subject>Phosphorylation</subject><subject>Protein Binding</subject><subject>Protein Interaction Mapping</subject><subject>Protein Processing, Post-Translational</subject><subject>Protein Structure, Tertiary</subject><subject>Protein Transport</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Psychomotor Performance - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, N-Methyl-D-Aspartate - analysis</subject><subject>Receptors, N-Methyl-D-Aspartate - chemistry</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Recombinant Fusion Proteins - pharmacology</subject><subject>Recombinant Fusion Proteins - therapeutic use</subject><subject>Subcellular Fractions - chemistry</subject><subject>Synapses - chemistry</subject><issn>0270-6474</issn><issn>1529-2401</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUFvEzEQhS0EomnhL1Q-wWnTsb32ri9IIS1tSmhQIWfLuztpDBtvsTdd9d_XaaICp5FmvnnzNI-QUwZjJrk4u765WN4ufkxnYym4ykCOOYB6RUZpqjOeA3tNRsALyFRe5EfkOMZfAFAAK96SI6ZkDlKVI3I9odPgelfbls58j8HWves8rbAfED29ueWfqfUN_Ta5XH6lztN5dr74Pklws62xoeeP8bfzGJ19R96sbBvx_aGekOWXi5_Tq2y-uJxNJ_OsljrvM6Flw8rSVjnaZxfQMMYbUGg1Vsl56lrQpcJc1JJVdlWUXCvGRbPiWoI4IZ_2uvfbaoNNjb4PtjX3wW1seDSddeb_iXdrc9c9GKUKoQuVBD4cBEL3Z4uxNxsXa2xb67HbRsMKKLUAmUC1B-vQxRhw9XKEgdnFYF5iMLsYDEiziyEtnv5r8e_a4e8J-LgH1u5uPbiAJm5s2yacmWEYkhRjhmuWiydG2JAW</recordid><startdate>20060315</startdate><enddate>20060315</enddate><creator>Gardoni, Fabrizio</creator><creator>Picconi, Barbara</creator><creator>Ghiglieri, Veronica</creator><creator>Polli, Federica</creator><creator>Bagetta, Vincenza</creator><creator>Bernardi, Giorgio</creator><creator>Cattabeni, Flaminio</creator><creator>Di Luca, Monica</creator><creator>Calabresi, Paolo</creator><general>Soc Neuroscience</general><general>Society for Neuroscience</general><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>7QG</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20060315</creationdate><title>A Critical Interaction between NR2B and MAGUK in L-DOPA Induced Dyskinesia</title><author>Gardoni, Fabrizio ; Picconi, Barbara ; Ghiglieri, Veronica ; Polli, Federica ; Bagetta, Vincenza ; Bernardi, Giorgio ; Cattabeni, Flaminio ; Di Luca, Monica ; Calabresi, Paolo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c594t-395d188ab4ea540560d112d06ea9eb240a54a0986e43c51baf78296123df29503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adaptor Proteins, Signal Transducing - chemistry</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Animals</topic><topic>Antiparkinson Agents - therapeutic use</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2</topic><topic>Calcium-Calmodulin-Dependent Protein Kinases - metabolism</topic><topic>Corpus Striatum - chemistry</topic><topic>Corpus Striatum - ultrastructure</topic><topic>Disks Large Homolog 4 Protein</topic><topic>Intracellular Signaling Peptides and Proteins - chemistry</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Levodopa - therapeutic use</topic><topic>Male</topic><topic>Membrane Proteins - chemistry</topic><topic>Membrane Proteins - metabolism</topic><topic>Motor Activity - drug effects</topic><topic>Neuropeptides - chemistry</topic><topic>Neuropeptides - metabolism</topic><topic>Oxidopamine - toxicity</topic><topic>Parkinsonian Disorders - chemically induced</topic><topic>Parkinsonian Disorders - drug therapy</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Parkinsonian Disorders - pathology</topic><topic>Phosphorylation</topic><topic>Protein Binding</topic><topic>Protein Interaction Mapping</topic><topic>Protein Processing, Post-Translational</topic><topic>Protein Structure, Tertiary</topic><topic>Protein Transport</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Psychomotor Performance - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, N-Methyl-D-Aspartate - analysis</topic><topic>Receptors, N-Methyl-D-Aspartate - chemistry</topic><topic>Receptors, N-Methyl-D-Aspartate - metabolism</topic><topic>Recombinant Fusion Proteins - pharmacology</topic><topic>Recombinant Fusion Proteins - therapeutic use</topic><topic>Subcellular Fractions - chemistry</topic><topic>Synapses - chemistry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gardoni, Fabrizio</creatorcontrib><creatorcontrib>Picconi, Barbara</creatorcontrib><creatorcontrib>Ghiglieri, Veronica</creatorcontrib><creatorcontrib>Polli, Federica</creatorcontrib><creatorcontrib>Bagetta, Vincenza</creatorcontrib><creatorcontrib>Bernardi, Giorgio</creatorcontrib><creatorcontrib>Cattabeni, Flaminio</creatorcontrib><creatorcontrib>Di Luca, Monica</creatorcontrib><creatorcontrib>Calabresi, Paolo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gardoni, Fabrizio</au><au>Picconi, Barbara</au><au>Ghiglieri, Veronica</au><au>Polli, Federica</au><au>Bagetta, Vincenza</au><au>Bernardi, Giorgio</au><au>Cattabeni, Flaminio</au><au>Di Luca, Monica</au><au>Calabresi, Paolo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Critical Interaction between NR2B and MAGUK in L-DOPA Induced Dyskinesia</atitle><jtitle>The Journal of neuroscience</jtitle><addtitle>J Neurosci</addtitle><date>2006-03-15</date><risdate>2006</risdate><volume>26</volume><issue>11</issue><spage>2914</spage><epage>2922</epage><pages>2914-2922</pages><issn>0270-6474</issn><eissn>1529-2401</eissn><abstract>Abnormal function of NMDA receptor has been suggested to be correlated with the pathogenesis of Parkinson's disease (PD) as well as with the development of l-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesia. Here we show that NMDA receptor NR2 subunits display specific alterations of their subcellular distribution in striata from unilateral 6-hydroxydopamine-lesioned, L-DOPA-treated dyskinetic, and L-DOPA-treated nondyskinetic rats. Dyskinetic animals have significantly higher levels of NR2A subunit in the postsynaptic compartment than all other experimental groups, whereas NR2B subunit shows a significant reduction in both dopamine-denervated and dyskinetic rats. These events are paralleled by profound modifications of NMDA receptor NR2B subunit association with interacting elements, i.e., members of the membrane-associated guanylate kinase (MAGUK) protein family postsynaptic density-95, synapse-associated protein-97 and synapse-associated protein-102. Treatment of nondyskinetic animals with a synthetic peptide (TAT2B) able to affect NR2B binding to MAGUK proteins as well as synaptic localization of this subunit in nondyskinetic rats was sufficient to induce a shift of treated rats toward a dyskinetic motor behavior. These data indicate abnormal NR2B redistribution between synaptic and extrasynaptic membranes as an important molecular disturbance of the glutamatergic synapse involved in L-DOPA-induced dyskinesia.</abstract><cop>United States</cop><pub>Soc Neuroscience</pub><pmid>16540568</pmid><doi>10.1523/JNEUROSCI.5326-05.2006</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - chemistry Adaptor Proteins, Signal Transducing - metabolism Animals Antiparkinson Agents - therapeutic use Calcium-Calmodulin-Dependent Protein Kinase Type 2 Calcium-Calmodulin-Dependent Protein Kinases - metabolism Corpus Striatum - chemistry Corpus Striatum - ultrastructure Disks Large Homolog 4 Protein Intracellular Signaling Peptides and Proteins - chemistry Intracellular Signaling Peptides and Proteins - metabolism Levodopa - therapeutic use Male Membrane Proteins - chemistry Membrane Proteins - metabolism Motor Activity - drug effects Neuropeptides - chemistry Neuropeptides - metabolism Oxidopamine - toxicity Parkinsonian Disorders - chemically induced Parkinsonian Disorders - drug therapy Parkinsonian Disorders - metabolism Parkinsonian Disorders - pathology Phosphorylation Protein Binding Protein Interaction Mapping Protein Processing, Post-Translational Protein Structure, Tertiary Protein Transport Protein-Tyrosine Kinases - metabolism Psychomotor Performance - drug effects Rats Rats, Wistar Receptors, N-Methyl-D-Aspartate - analysis Receptors, N-Methyl-D-Aspartate - chemistry Receptors, N-Methyl-D-Aspartate - metabolism Recombinant Fusion Proteins - pharmacology Recombinant Fusion Proteins - therapeutic use Subcellular Fractions - chemistry Synapses - chemistry |
| title | A Critical Interaction between NR2B and MAGUK in L-DOPA Induced Dyskinesia |
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