Src-protein tyrosine kinases are required for cocaine-induced increase in the expression and function of the NMDA receptor in the ventral tegmental area
Cocaine-induced long-term potentiation of glutamatergic synapses in the ventral tegmental area (VTA) has been proposed as a key process that contributes to the development of addictive behaviors. In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for...
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| description | Cocaine-induced long-term potentiation of glutamatergic synapses in the ventral tegmental area (VTA) has been proposed as a key process that contributes to the development of addictive behaviors. In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for the initiation of cocaine sensitization. Here we show that application of cocaine both in slices and in vivo induced an increase in tyrosine phosphorylation of the NR2A, but not the NR2B subunit of the NMDAR in juvenile rats. Cocaine induced an increase in the activity of both Fyn and Src kinases, and the Src-protein tyrosine kinase (Src-PTKs) inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), abolished both cocaine-induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA. Moreover, cocaine-induced enhancement in NMDAR-mediated excitatory post-synaptic currents was completely abolished by PP2. Taken together, these results suggest that acute cocaine induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A-containing NMDAR through members of the Src-PTKs. This in turn, increased NMDAR-mediated currents in VTA dopamine neurons. These results provide a potential cellular mechanism by which cocaine triggers NMDAR-dependent synaptic plasticity of VTA neurons that may underlie the development of behavioral sensitization. |
| doi_str_mv | 10.1111/j.1471-4159.2008.05794.x |
| format | Article |
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In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for the initiation of cocaine sensitization. Here we show that application of cocaine both in slices and in vivo induced an increase in tyrosine phosphorylation of the NR2A, but not the NR2B subunit of the NMDAR in juvenile rats. Cocaine induced an increase in the activity of both Fyn and Src kinases, and the Src-protein tyrosine kinase (Src-PTKs) inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), abolished both cocaine-induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA. Moreover, cocaine-induced enhancement in NMDAR-mediated excitatory post-synaptic currents was completely abolished by PP2. Taken together, these results suggest that acute cocaine induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A-containing NMDAR through members of the Src-PTKs. This in turn, increased NMDAR-mediated currents in VTA dopamine neurons. These results provide a potential cellular mechanism by which cocaine triggers NMDAR-dependent synaptic plasticity of VTA neurons that may underlie the development of behavioral sensitization.</description><identifier>ISSN: 0022-3042</identifier><identifier>EISSN: 1471-4159</identifier><identifier>DOI: 10.1111/j.1471-4159.2008.05794.x</identifier><identifier>PMID: 19046409</identifier><identifier>CODEN: JONRA9</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Addictions ; Addictive behaviors ; Adult and adolescent clinical studies ; Animals ; Biochemistry ; Biological and medical sciences ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cocaine ; Cocaine - pharmacology ; Dopamine Uptake Inhibitors - pharmacology ; Drug addiction ; Electrophysiology ; Excitatory Postsynaptic Potentials - drug effects ; Fundamental and applied biological sciences. Psychology ; Indicators and Reagents ; Long-Term Potentiation - drug effects ; Male ; Medical sciences ; Neurology ; Neurotransmitters ; NMDA receptors ; Patch-Clamp Techniques ; Phosphorylation ; Proto-Oncogene Proteins c-fyn - biosynthesis ; Proto-Oncogene Proteins c-fyn - genetics ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Rats ; Receptors, N-Methyl-D-Aspartate - biosynthesis ; Receptors, N-Methyl-D-Aspartate - drug effects ; Receptors, N-Methyl-D-Aspartate - genetics ; Src protein tyrosine kinase ; src-Family Kinases - metabolism ; Subcellular Fractions - drug effects ; Tyrosine - metabolism ; tyrosine phosphorylation ; ventral tegmental area ; Ventral Tegmental Area - drug effects ; Ventral Tegmental Area - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurochemistry, 2009-02, Vol.108 (3), p.697-706</ispartof><rights>2008 The Authors. Journal Compilation © 2008 International Society for Neurochemistry</rights><rights>2009 INIST-CNRS</rights><rights>Journal compilation © 2009 International Society for Neurochemistry</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5294-341cdb677268103e3fabed92703b6a712e6cb6a2d3124771195feb6957115b883</citedby><cites>FETCH-LOGICAL-c5294-341cdb677268103e3fabed92703b6a712e6cb6a2d3124771195feb6957115b883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1471-4159.2008.05794.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1471-4159.2008.05794.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21031087$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19046409$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schumann, Johanna</creatorcontrib><creatorcontrib>Michaeli, Avner</creatorcontrib><creatorcontrib>Yaka, Rami</creatorcontrib><title>Src-protein tyrosine kinases are required for cocaine-induced increase in the expression and function of the NMDA receptor in the ventral tegmental area</title><title>Journal of neurochemistry</title><addtitle>J Neurochem</addtitle><description>Cocaine-induced long-term potentiation of glutamatergic synapses in the ventral tegmental area (VTA) has been proposed as a key process that contributes to the development of addictive behaviors. In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for the initiation of cocaine sensitization. Here we show that application of cocaine both in slices and in vivo induced an increase in tyrosine phosphorylation of the NR2A, but not the NR2B subunit of the NMDAR in juvenile rats. Cocaine induced an increase in the activity of both Fyn and Src kinases, and the Src-protein tyrosine kinase (Src-PTKs) inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), abolished both cocaine-induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA. Moreover, cocaine-induced enhancement in NMDAR-mediated excitatory post-synaptic currents was completely abolished by PP2. Taken together, these results suggest that acute cocaine induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A-containing NMDAR through members of the Src-PTKs. This in turn, increased NMDAR-mediated currents in VTA dopamine neurons. These results provide a potential cellular mechanism by which cocaine triggers NMDAR-dependent synaptic plasticity of VTA neurons that may underlie the development of behavioral sensitization.</description><subject>Addictions</subject><subject>Addictive behaviors</subject><subject>Adult and adolescent clinical studies</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cocaine</subject><subject>Cocaine - pharmacology</subject><subject>Dopamine Uptake Inhibitors - pharmacology</subject><subject>Drug addiction</subject><subject>Electrophysiology</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Indicators and Reagents</subject><subject>Long-Term Potentiation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Neurotransmitters</subject><subject>NMDA receptors</subject><subject>Patch-Clamp Techniques</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-fyn - biosynthesis</subject><subject>Proto-Oncogene Proteins c-fyn - genetics</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Rats</subject><subject>Receptors, N-Methyl-D-Aspartate - biosynthesis</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, N-Methyl-D-Aspartate - genetics</subject><subject>Src protein tyrosine kinase</subject><subject>src-Family Kinases - metabolism</subject><subject>Subcellular Fractions - drug effects</subject><subject>Tyrosine - metabolism</subject><subject>tyrosine phosphorylation</subject><subject>ventral tegmental area</subject><subject>Ventral Tegmental Area - drug effects</subject><subject>Ventral Tegmental Area - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3042</issn><issn>1471-4159</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhSMEokPhFcBCgl0G_ztZsKiGf5WyKF1bjnNTPGScqZ3AzJvwuNx0RkViA9742P7OtX1PURBGlwzHq_WSScNKyVS95JRWS6pMLZe7e8Xi7uB-saCU81JQyU-KRzmvKWVaavawOGE1lVrSelH8uky-3KZhhBDJuE9DDhHI9xBdhkxcApLgZgoJWtINifjBOwTKENvJ416IPgGiZHZ_AwK7bYKcwxCJi2iZoh_nxdDdHl98fnOGBT1sRyx29PyAOCbXkxGuNyhR4bXucfGgc32GJ8f5tLh69_br6kN5_uX9x9XZeekVr2UpJPNto43humJUgOhcA23NDRWNdoZx0B4FbwXj0hjGatVBo2uFUjVVJU6Ll4e62ISbCfJoNyF76HsXYZiy1boySkjzT5BTIRXjHMHnf4HrYUoRP4GMVlQyIRGqDpDHlucEnd2msHFpbxm1c8Z2beco7RylnTO2txnbHVqfHutPzQbaP8ZjqAi8OAIue9d3yUUf8h3HsU-MVvOPXh-4n6GH_X8_wH66WM0K_c8O_s4N1l0nvOPqklMmKFOmqlQlfgNGecvC</recordid><startdate>200902</startdate><enddate>200902</enddate><creator>Schumann, Johanna</creator><creator>Michaeli, Avner</creator><creator>Yaka, Rami</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>FBQ</scope><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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200902</creationdate><title>Src-protein tyrosine kinases are required for cocaine-induced increase in the expression and function of the NMDA receptor in the ventral tegmental area</title><author>Schumann, Johanna ; Michaeli, Avner ; Yaka, Rami</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5294-341cdb677268103e3fabed92703b6a712e6cb6a2d3124771195feb6957115b883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Addictions</topic><topic>Addictive behaviors</topic><topic>Adult and adolescent clinical studies</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biological and medical sciences</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cocaine</topic><topic>Cocaine - pharmacology</topic><topic>Dopamine Uptake Inhibitors - pharmacology</topic><topic>Drug addiction</topic><topic>Electrophysiology</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Indicators and Reagents</topic><topic>Long-Term Potentiation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Neurotransmitters</topic><topic>NMDA receptors</topic><topic>Patch-Clamp Techniques</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-fyn - biosynthesis</topic><topic>Proto-Oncogene Proteins c-fyn - genetics</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Rats</topic><topic>Receptors, N-Methyl-D-Aspartate - biosynthesis</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, N-Methyl-D-Aspartate - genetics</topic><topic>Src protein tyrosine kinase</topic><topic>src-Family Kinases - metabolism</topic><topic>Subcellular Fractions - drug effects</topic><topic>Tyrosine - metabolism</topic><topic>tyrosine phosphorylation</topic><topic>ventral tegmental area</topic><topic>Ventral Tegmental Area - drug effects</topic><topic>Ventral Tegmental Area - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schumann, Johanna</creatorcontrib><creatorcontrib>Michaeli, Avner</creatorcontrib><creatorcontrib>Yaka, Rami</creatorcontrib><collection>AGRIS</collection><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schumann, Johanna</au><au>Michaeli, Avner</au><au>Yaka, Rami</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Src-protein tyrosine kinases are required for cocaine-induced increase in the expression and function of the NMDA receptor in the ventral tegmental area</atitle><jtitle>Journal of neurochemistry</jtitle><addtitle>J Neurochem</addtitle><date>2009-02</date><risdate>2009</risdate><volume>108</volume><issue>3</issue><spage>697</spage><epage>706</epage><pages>697-706</pages><issn>0022-3042</issn><eissn>1471-4159</eissn><coden>JONRA9</coden><abstract>Cocaine-induced long-term potentiation of glutamatergic synapses in the ventral tegmental area (VTA) has been proposed as a key process that contributes to the development of addictive behaviors. In particular, the activation of ionotrophic glutamate NMDA receptor (NMDAR) in the VTA is critical for the initiation of cocaine sensitization. Here we show that application of cocaine both in slices and in vivo induced an increase in tyrosine phosphorylation of the NR2A, but not the NR2B subunit of the NMDAR in juvenile rats. Cocaine induced an increase in the activity of both Fyn and Src kinases, and the Src-protein tyrosine kinase (Src-PTKs) inhibitor, 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), abolished both cocaine-induced increase in tyrosine phosphorylation of the NR2A subunit and the increase in the expression of NR1, NR2A, and NR2B in the VTA. Moreover, cocaine-induced enhancement in NMDAR-mediated excitatory post-synaptic currents was completely abolished by PP2. Taken together, these results suggest that acute cocaine induced an increase in the expression of NMDAR subunits and enhanced tyrosine phosphorylation of NR2A-containing NMDAR through members of the Src-PTKs. This in turn, increased NMDAR-mediated currents in VTA dopamine neurons. These results provide a potential cellular mechanism by which cocaine triggers NMDAR-dependent synaptic plasticity of VTA neurons that may underlie the development of behavioral sensitization.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>19046409</pmid><doi>10.1111/j.1471-4159.2008.05794.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Addictions Addictive behaviors Adult and adolescent clinical studies Animals Biochemistry Biological and medical sciences Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cocaine Cocaine - pharmacology Dopamine Uptake Inhibitors - pharmacology Drug addiction Electrophysiology Excitatory Postsynaptic Potentials - drug effects Fundamental and applied biological sciences. Psychology Indicators and Reagents Long-Term Potentiation - drug effects Male Medical sciences Neurology Neurotransmitters NMDA receptors Patch-Clamp Techniques Phosphorylation Proto-Oncogene Proteins c-fyn - biosynthesis Proto-Oncogene Proteins c-fyn - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Rats Receptors, N-Methyl-D-Aspartate - biosynthesis Receptors, N-Methyl-D-Aspartate - drug effects Receptors, N-Methyl-D-Aspartate - genetics Src protein tyrosine kinase src-Family Kinases - metabolism Subcellular Fractions - drug effects Tyrosine - metabolism tyrosine phosphorylation ventral tegmental area Ventral Tegmental Area - drug effects Ventral Tegmental Area - metabolism Vertebrates: nervous system and sense organs |
| title | Src-protein tyrosine kinases are required for cocaine-induced increase in the expression and function of the NMDA receptor in the ventral tegmental area |
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