Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation
The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson’s disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor’s downstream signal...
Gespeichert in:
| Veröffentlicht in: | Molecular psychiatry 2020-09, Vol.25 (9), p.2086-2100 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2100 |
|---|---|
| container_issue | 9 |
| container_start_page | 2086 |
| container_title | Molecular psychiatry |
| container_volume | 25 |
| creator | Donthamsetti, Prashant Gallo, Eduardo F. Buck, David C. Stahl, Edward L. Zhu, Ying Lane, J. Robert Bohn, Laura M. Neve, Kim A. Kellendonk, Christoph Javitch, Jonathan A. |
| description | The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson’s disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor’s downstream signaling processes in vivo and how these relate to the desired and undesired effects of drugs. D2R is a G protein-coupled receptor (GPCR) that activates G protein-dependent as well as non-canonical arrestin-dependent signaling pathways. Whether these effector pathways act alone or in concert to facilitate specific D2R-dependent behaviors is unclear. Here, we report on the development of a D2R mutant that recruits arrestin but is devoid of G protein activity. When expressed virally in “indirect pathway” medium spiny neurons (iMSNs) in the ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence of D2R-mediated G protein signaling. In contrast, incentive motivation was enhanced only by wild-type D2R, signifying a dissociation in the mechanisms that underlie distinct D2R-dependent behaviors, and opening the door to more targeted therapeutics. |
| doi_str_mv | 10.1038/s41380-018-0212-4 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6378141</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A634552643</galeid><sourcerecordid>A634552643</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-4ff172edd50c91c2dbafc36dd973e6f532f738f0c7073c80dccf3702f695b7243</originalsourceid><addsrcrecordid>eNqFUk2LFDEUDKK46-gP8CIBL156zXfSF2FYdRUW9qJHCZl0MmbpTsYkPbD_3jSzn7KL5JCQqnp5r1IAvMXoBCOqPhaGqUIdwqpDBJOOPQPHmEnRcS7V83amvO8YVuwIvCrlEqEF5C_BEUWYoCY-Br_WObtSQ4TZ2TyHOrlYYU1wSDszhejgZ7JAbldThpMbgqmuwDHZNKUaUoSbucKYKgzRNmnYO7gAe7OAr8ELb8bi3lzvK_Dz65cfp9-684uz76fr885ywWvHvMeSuGHgyPbYkmFjvKViGHpJnfCcEi-p8shKJKlVaLDWU4mIFz3fSMLoCnw61N3Nm9bj0kg2o97lMJl8pZMJ-iESw2-9TXstqFS4GbECH64L5PRnboboKRTrxtFEl-aiCVK9EqjveaO-_4d6meYc23iaNHslFYT_h8Xab2EuyR1ra0anQ_SpdWeXp_VaUMY5EYw21skjrLYGNwWbovOh3T8Q4IPA5lRKdv7WCYz0khx9SI5uydFLcvRi4bv7Ft4qbqLSCORAKA2KW5fvJnq66l9qk83I</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2440211572</pqid></control><display><type>article</type><title>Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Donthamsetti, Prashant ; Gallo, Eduardo F. ; Buck, David C. ; Stahl, Edward L. ; Zhu, Ying ; Lane, J. Robert ; Bohn, Laura M. ; Neve, Kim A. ; Kellendonk, Christoph ; Javitch, Jonathan A.</creator><creatorcontrib>Donthamsetti, Prashant ; Gallo, Eduardo F. ; Buck, David C. ; Stahl, Edward L. ; Zhu, Ying ; Lane, J. Robert ; Bohn, Laura M. ; Neve, Kim A. ; Kellendonk, Christoph ; Javitch, Jonathan A.</creatorcontrib><description>The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson’s disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor’s downstream signaling processes in vivo and how these relate to the desired and undesired effects of drugs. D2R is a G protein-coupled receptor (GPCR) that activates G protein-dependent as well as non-canonical arrestin-dependent signaling pathways. Whether these effector pathways act alone or in concert to facilitate specific D2R-dependent behaviors is unclear. Here, we report on the development of a D2R mutant that recruits arrestin but is devoid of G protein activity. When expressed virally in “indirect pathway” medium spiny neurons (iMSNs) in the ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence of D2R-mediated G protein signaling. In contrast, incentive motivation was enhanced only by wild-type D2R, signifying a dissociation in the mechanisms that underlie distinct D2R-dependent behaviors, and opening the door to more targeted therapeutics.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/s41380-018-0212-4</identifier><identifier>PMID: 30120413</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/106 ; 13/109 ; 13/31 ; 13/51 ; 13/95 ; 14 ; 14/1 ; 14/35 ; 14/63 ; 38/23 ; 38/70 ; 38/77 ; 59 ; 631/378 ; 64 ; 64/60 ; 692/699/476/1311 ; 692/699/476/1799 ; 692/699/476/5 ; 82 ; 9/10 ; 96 ; Animals ; Arrestin ; Behavioral Sciences ; Biological Psychology ; Cocaine ; Corpus Striatum - metabolism ; Dopamine ; Dopamine D2 receptors ; Employee incentives ; G protein-coupled receptors ; G proteins ; Health aspects ; Locomotion ; Locomotor activity ; Medicine ; Medicine & Public Health ; Membrane proteins ; Mental disorders ; Mice ; Mice, Knockout ; Motivation ; Movement disorders ; Mutants ; Neostriatum ; Nervous system diseases ; Neurodegenerative diseases ; Neurosciences ; Parkinson's disease ; Pharmacotherapy ; Phenols ; Proteins ; Psychiatry ; Receptors, Dopamine D2 - genetics ; Receptors, Dopamine D2 - metabolism ; Schizophrenia ; Signal transduction ; Spiny neurons ; Tetracycline ; Tetracyclines</subject><ispartof>Molecular psychiatry, 2020-09, Vol.25 (9), p.2086-2100</ispartof><rights>Springer Nature Limited 2018</rights><rights>COPYRIGHT 2020 Nature Publishing Group</rights><rights>Springer Nature Limited 2018.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-4ff172edd50c91c2dbafc36dd973e6f532f738f0c7073c80dccf3702f695b7243</citedby><cites>FETCH-LOGICAL-c565t-4ff172edd50c91c2dbafc36dd973e6f532f738f0c7073c80dccf3702f695b7243</cites><orcidid>0000-0001-7395-2967</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41380-018-0212-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41380-018-0212-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30120413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Donthamsetti, Prashant</creatorcontrib><creatorcontrib>Gallo, Eduardo F.</creatorcontrib><creatorcontrib>Buck, David C.</creatorcontrib><creatorcontrib>Stahl, Edward L.</creatorcontrib><creatorcontrib>Zhu, Ying</creatorcontrib><creatorcontrib>Lane, J. Robert</creatorcontrib><creatorcontrib>Bohn, Laura M.</creatorcontrib><creatorcontrib>Neve, Kim A.</creatorcontrib><creatorcontrib>Kellendonk, Christoph</creatorcontrib><creatorcontrib>Javitch, Jonathan A.</creatorcontrib><title>Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson’s disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor’s downstream signaling processes in vivo and how these relate to the desired and undesired effects of drugs. D2R is a G protein-coupled receptor (GPCR) that activates G protein-dependent as well as non-canonical arrestin-dependent signaling pathways. Whether these effector pathways act alone or in concert to facilitate specific D2R-dependent behaviors is unclear. Here, we report on the development of a D2R mutant that recruits arrestin but is devoid of G protein activity. When expressed virally in “indirect pathway” medium spiny neurons (iMSNs) in the ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence of D2R-mediated G protein signaling. In contrast, incentive motivation was enhanced only by wild-type D2R, signifying a dissociation in the mechanisms that underlie distinct D2R-dependent behaviors, and opening the door to more targeted therapeutics.</description><subject>13/1</subject><subject>13/106</subject><subject>13/109</subject><subject>13/31</subject><subject>13/51</subject><subject>13/95</subject><subject>14</subject><subject>14/1</subject><subject>14/35</subject><subject>14/63</subject><subject>38/23</subject><subject>38/70</subject><subject>38/77</subject><subject>59</subject><subject>631/378</subject><subject>64</subject><subject>64/60</subject><subject>692/699/476/1311</subject><subject>692/699/476/1799</subject><subject>692/699/476/5</subject><subject>82</subject><subject>9/10</subject><subject>96</subject><subject>Animals</subject><subject>Arrestin</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Cocaine</subject><subject>Corpus Striatum - metabolism</subject><subject>Dopamine</subject><subject>Dopamine D2 receptors</subject><subject>Employee incentives</subject><subject>G protein-coupled receptors</subject><subject>G proteins</subject><subject>Health aspects</subject><subject>Locomotion</subject><subject>Locomotor activity</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane proteins</subject><subject>Mental disorders</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Motivation</subject><subject>Movement disorders</subject><subject>Mutants</subject><subject>Neostriatum</subject><subject>Nervous system diseases</subject><subject>Neurodegenerative diseases</subject><subject>Neurosciences</subject><subject>Parkinson's disease</subject><subject>Pharmacotherapy</subject><subject>Phenols</subject><subject>Proteins</subject><subject>Psychiatry</subject><subject>Receptors, Dopamine D2 - genetics</subject><subject>Receptors, Dopamine D2 - metabolism</subject><subject>Schizophrenia</subject><subject>Signal transduction</subject><subject>Spiny neurons</subject><subject>Tetracycline</subject><subject>Tetracyclines</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFUk2LFDEUDKK46-gP8CIBL156zXfSF2FYdRUW9qJHCZl0MmbpTsYkPbD_3jSzn7KL5JCQqnp5r1IAvMXoBCOqPhaGqUIdwqpDBJOOPQPHmEnRcS7V83amvO8YVuwIvCrlEqEF5C_BEUWYoCY-Br_WObtSQ4TZ2TyHOrlYYU1wSDszhejgZ7JAbldThpMbgqmuwDHZNKUaUoSbucKYKgzRNmnYO7gAe7OAr8ELb8bi3lzvK_Dz65cfp9-684uz76fr885ywWvHvMeSuGHgyPbYkmFjvKViGHpJnfCcEi-p8shKJKlVaLDWU4mIFz3fSMLoCnw61N3Nm9bj0kg2o97lMJl8pZMJ-iESw2-9TXstqFS4GbECH64L5PRnboboKRTrxtFEl-aiCVK9EqjveaO-_4d6meYc23iaNHslFYT_h8Xab2EuyR1ra0anQ_SpdWeXp_VaUMY5EYw21skjrLYGNwWbovOh3T8Q4IPA5lRKdv7WCYz0khx9SI5uydFLcvRi4bv7Ft4qbqLSCORAKA2KW5fvJnq66l9qk83I</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Donthamsetti, Prashant</creator><creator>Gallo, Eduardo F.</creator><creator>Buck, David C.</creator><creator>Stahl, Edward L.</creator><creator>Zhu, Ying</creator><creator>Lane, J. Robert</creator><creator>Bohn, Laura M.</creator><creator>Neve, Kim A.</creator><creator>Kellendonk, Christoph</creator><creator>Javitch, Jonathan A.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7395-2967</orcidid></search><sort><creationdate>20200901</creationdate><title>Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation</title><author>Donthamsetti, Prashant ; Gallo, Eduardo F. ; Buck, David C. ; Stahl, Edward L. ; Zhu, Ying ; Lane, J. Robert ; Bohn, Laura M. ; Neve, Kim A. ; Kellendonk, Christoph ; Javitch, Jonathan A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-4ff172edd50c91c2dbafc36dd973e6f532f738f0c7073c80dccf3702f695b7243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/1</topic><topic>13/106</topic><topic>13/109</topic><topic>13/31</topic><topic>13/51</topic><topic>13/95</topic><topic>14</topic><topic>14/1</topic><topic>14/35</topic><topic>14/63</topic><topic>38/23</topic><topic>38/70</topic><topic>38/77</topic><topic>59</topic><topic>631/378</topic><topic>64</topic><topic>64/60</topic><topic>692/699/476/1311</topic><topic>692/699/476/1799</topic><topic>692/699/476/5</topic><topic>82</topic><topic>9/10</topic><topic>96</topic><topic>Animals</topic><topic>Arrestin</topic><topic>Behavioral Sciences</topic><topic>Biological Psychology</topic><topic>Cocaine</topic><topic>Corpus Striatum - metabolism</topic><topic>Dopamine</topic><topic>Dopamine D2 receptors</topic><topic>Employee incentives</topic><topic>G protein-coupled receptors</topic><topic>G proteins</topic><topic>Health aspects</topic><topic>Locomotion</topic><topic>Locomotor activity</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane proteins</topic><topic>Mental disorders</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Motivation</topic><topic>Movement disorders</topic><topic>Mutants</topic><topic>Neostriatum</topic><topic>Nervous system diseases</topic><topic>Neurodegenerative diseases</topic><topic>Neurosciences</topic><topic>Parkinson's disease</topic><topic>Pharmacotherapy</topic><topic>Phenols</topic><topic>Proteins</topic><topic>Psychiatry</topic><topic>Receptors, Dopamine D2 - genetics</topic><topic>Receptors, Dopamine D2 - metabolism</topic><topic>Schizophrenia</topic><topic>Signal transduction</topic><topic>Spiny neurons</topic><topic>Tetracycline</topic><topic>Tetracyclines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Donthamsetti, Prashant</creatorcontrib><creatorcontrib>Gallo, Eduardo F.</creatorcontrib><creatorcontrib>Buck, David C.</creatorcontrib><creatorcontrib>Stahl, Edward L.</creatorcontrib><creatorcontrib>Zhu, Ying</creatorcontrib><creatorcontrib>Lane, J. Robert</creatorcontrib><creatorcontrib>Bohn, Laura M.</creatorcontrib><creatorcontrib>Neve, Kim A.</creatorcontrib><creatorcontrib>Kellendonk, Christoph</creatorcontrib><creatorcontrib>Javitch, Jonathan A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Donthamsetti, Prashant</au><au>Gallo, Eduardo F.</au><au>Buck, David C.</au><au>Stahl, Edward L.</au><au>Zhu, Ying</au><au>Lane, J. Robert</au><au>Bohn, Laura M.</au><au>Neve, Kim A.</au><au>Kellendonk, Christoph</au><au>Javitch, Jonathan A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>25</volume><issue>9</issue><spage>2086</spage><epage>2100</epage><pages>2086-2100</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson’s disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor’s downstream signaling processes in vivo and how these relate to the desired and undesired effects of drugs. D2R is a G protein-coupled receptor (GPCR) that activates G protein-dependent as well as non-canonical arrestin-dependent signaling pathways. Whether these effector pathways act alone or in concert to facilitate specific D2R-dependent behaviors is unclear. Here, we report on the development of a D2R mutant that recruits arrestin but is devoid of G protein activity. When expressed virally in “indirect pathway” medium spiny neurons (iMSNs) in the ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence of D2R-mediated G protein signaling. In contrast, incentive motivation was enhanced only by wild-type D2R, signifying a dissociation in the mechanisms that underlie distinct D2R-dependent behaviors, and opening the door to more targeted therapeutics.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30120413</pmid><doi>10.1038/s41380-018-0212-4</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-7395-2967</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1359-4184 |
| ispartof | Molecular psychiatry, 2020-09, Vol.25 (9), p.2086-2100 |
| issn | 1359-4184 1476-5578 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6378141 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | 13/1 13/106 13/109 13/31 13/51 13/95 14 14/1 14/35 14/63 38/23 38/70 38/77 59 631/378 64 64/60 692/699/476/1311 692/699/476/1799 692/699/476/5 82 9/10 96 Animals Arrestin Behavioral Sciences Biological Psychology Cocaine Corpus Striatum - metabolism Dopamine Dopamine D2 receptors Employee incentives G protein-coupled receptors G proteins Health aspects Locomotion Locomotor activity Medicine Medicine & Public Health Membrane proteins Mental disorders Mice Mice, Knockout Motivation Movement disorders Mutants Neostriatum Nervous system diseases Neurodegenerative diseases Neurosciences Parkinson's disease Pharmacotherapy Phenols Proteins Psychiatry Receptors, Dopamine D2 - genetics Receptors, Dopamine D2 - metabolism Schizophrenia Signal transduction Spiny neurons Tetracycline Tetracyclines |
| title | Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T07%3A47%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Arrestin%20recruitment%20to%20dopamine%20D2%20receptor%20mediates%20locomotion%20but%20not%20incentive%20motivation&rft.jtitle=Molecular%20psychiatry&rft.au=Donthamsetti,%20Prashant&rft.date=2020-09-01&rft.volume=25&rft.issue=9&rft.spage=2086&rft.epage=2100&rft.pages=2086-2100&rft.issn=1359-4184&rft.eissn=1476-5578&rft_id=info:doi/10.1038/s41380-018-0212-4&rft_dat=%3Cgale_pubme%3EA634552643%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2440211572&rft_id=info:pmid/30120413&rft_galeid=A634552643&rfr_iscdi=true |