{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T09:22:05Z","timestamp":1791105725562,"version":"4.1.0"},"reference-count":37,"publisher":"National Academy of Sciences","issue":"6","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2008,2,12]]},"abstract":"<jats:p>\n                    Parkinson's disease (PD) is characterized by a progressive degeneration of substantia nigra dopaminergic neurons projecting to the striatum. Restoration of dopamine transmission by\n                    <jats:sc>l<\/jats:sc>\n                    -DOPA relieves symptoms of PD but causes prominent side effects. There is a strong serotonin innervation of the striatum by serotonergic neurons that remains relatively preserved in PD. The study of this innervation has been largely neglected. Here, we demonstrate that chronic\n                    <jats:sc>l<\/jats:sc>\n                    -DOPA administration to 6-OHDA-lesioned rodents increases, via D\n                    <jats:sub>1<\/jats:sub>\n                    receptors, the levels of the 5-HT\n                    <jats:sub>1B<\/jats:sub>\n                    receptor and its adaptor protein, p11, in dopamine-denervated striatonigral neurons. Using unilaterally 6-OHDA-lesioned p11 WT and KO mice, it was found that administration of a selective 5-HT\n                    <jats:sub>1B<\/jats:sub>\n                    receptor agonist, CP94253, inhibited\n                    <jats:sc>l<\/jats:sc>\n                    -DOPA-induced rotational behavior and abnormal involuntary movements in a p11-dependent manner. These data reveal an\n                    <jats:sc>l<\/jats:sc>\n                    -DOPA-induced negative-feedback mechanism, whereby the serotonin system may influence the symptomatology of Parkinsonism.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0711839105","type":"journal-article","created":{"date-parts":[[2008,2,6]],"date-time":"2008-02-06T20:54:53Z","timestamp":1202331293000},"page":"2163-2168","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":103,"title":["Evidence for a role of the 5-HT\n                    <sub>1B<\/sub>\n                    receptor and its adaptor protein, p11, in\n                    <scp>l<\/scp>\n                    -DOPA treatment of an animal model of Parkinsonism"],"prefix":"10.1073","volume":"105","author":[{"given":"Xiaoqun","family":"Zhang","sequence":"first","affiliation":[{"name":"*Section of Translational Neuropharmacology, Department of Physiology and Pharmacology, Karolinska Institute, 17177 Stockholm, Sweden; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per E.","family":"Andren","sequence":"additional","affiliation":[{"name":"Laboratory for Biological and Medical Mass Spectrometry, Uppsala University, 75123 Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Greengard","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY10021;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per","family":"Svenningsson","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY10021;"},{"name":"*Section of Translational Neuropharmacology, Department of Physiology and Pharmacology, Karolinska Institute, 17177 Stockholm, Sweden; and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2008,2,12]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF01485901"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(03)00568-3"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa033447"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM196803142781127"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2147780"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.294.5544.1024"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2007.02.001"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20296"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0676-04.2004"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1992.tb10939.x"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/nn1040"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0852-07.2007"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1460-9568.1998.00285.x"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopsych.2005.05.044"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1006\/nbdi.1999.0259"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2007.04456.x"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)90486-0"},{"key":"e_1_3_3_18_2","first-page":"120","article-title":"Preferential loss of serotonin markers in caudate versus putamen in Parkinson's disease.","volume":"131","author":"Kish SJ","year":"2008","unstructured":"SJ Kish, et al., Preferential loss of serotonin markers in caudate versus putamen in Parkinson's disease. 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