{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T03:03:12Z","timestamp":1790996592784,"version":"4.1.0"},"reference-count":52,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T00:00:00Z","timestamp":1543363200000},"content-version":"vor","delay-in-days":27,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["movementdisorders.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2018,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    The serotonergic system is a well\u2010established modulator of\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia. To date, targeting serotonin transporters or serotonin receptor subtype 1A (5\u2010HT\n                    <jats:sub>1A<\/jats:sub>\n                    ) reduces\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia in animal models; however, these strategies have failed to translate clinically. Ideally, a compound acting at both known antidyskinetic sites could optimize serotonin\u2010mediated approaches. Vilazodone is a selective serotonin reuptake inhibitor and a partial 5\u2010HT\n                    <jats:sub>1A<\/jats:sub>\n                    agonist approved by the U.S. Food and Drug Administration, situating Vilazodone in a unique position to reduce\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia without compromising\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010mediated motor improvements.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Objectives<\/jats:bold>\n                    : The goal of the present study was to characterize Vilazodone's effects on\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced behaviors, neurochemistry and gene expression in unilateral 6\u2010hydroxydopamine\u2010lesioned hemi\u2010parkinsonian rats.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods<\/jats:bold>\n                    : In experiments 1 and 2,\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010na\u00efve and\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010primed animals were coadministered Vilazodone and\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa daily for 3 weeks to model subchronic use, and behavioral, neurochemical, and messenger RNA (mRNA) expression changes were measured. In experiment 3, dyskinetic behavior was assessed following 5\u2010HT\n                    <jats:sub>1A<\/jats:sub>\n                    or serotonin receptor subtype 1B blockade prior to Vilazodone\u2013\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa coadministration.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results<\/jats:bold>\n                    : Vilazodone significantly suppressed developing and established\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia without compromising the promotor effects of\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa therapy. In the dopamine\u2010depleted striatum, Vilazodone\u2013\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa cotreatment increased dopamine content, suggesting a normalization of dopamine kinetics in dyskinetic brain, and reduced\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced c\u2010Fos and preprodynorphin mRNA overexpression, indicative of attenuated dopamine D\n                    <jats:sub>1<\/jats:sub>\n                    receptor\u2010mediated direct pathway overactivity. Only 5\u2010HT\n                    <jats:sub>1A<\/jats:sub>\n                    antagonism partially attenuated Vilazodone's antidyskinetic efficacy, suggesting both serotonin transporter\u2010dependent effects and 5\u2010HT\n                    <jats:sub>1A<\/jats:sub>\n                    receptors in Vilazodone's actions.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusions<\/jats:bold>\n                    : Our findings show Vilazodone has a serotonin\u2010dependent effect on rodent\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia and implicate the potential for repositioning Vilazodone against\n                    <jats:sc>l<\/jats:sc>\n                    \u2010dopa\u2010induced dyskinesia development and expression in Parkinson's disease patients. \u00a9 2018 International Parkinson and Movement Disorder Society\n                  <\/jats:p>","DOI":"10.1002\/mds.100","type":"journal-article","created":{"date-parts":[[2018,11,28]],"date-time":"2018-11-28T17:37:16Z","timestamp":1543426636000},"page":"1740-1749","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Diverse serotonin actions of vilazodone reduce l\u20103,4\u2010dihidroxyphenylalanine\u2013induced dyskinesia in hemi\u2010parkinsonian rats"],"prefix":"10.1002","volume":"33","author":[{"given":"Samantha M.","family":"Meadows","sequence":"first","affiliation":[{"name":"Behavioral Neuroscience Program, Department of Psychology Binghamton University  Binghamton New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa M.","family":"Conti","sequence":"additional","affiliation":[{"name":"Behavioral Neuroscience Program, Department of Psychology Binghamton University  Binghamton New York 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