{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T06:28:03Z","timestamp":1790144883249,"version":"4.0.1"},"reference-count":51,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2019,5,14]],"date-time":"2019-05-14T00:00:00Z","timestamp":1557792000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    In monogenetic generalized forms of dystonia, in vitro neurophysiological recordings have demonstrated direct evidence for abnormal plasticity at the level of the cortico\u2010striatal synapse. It is unclear whether similar abnormalities contribute to the pathophysiology of cervical dystonia, the most common type of focal dystonia. We investigated whether abnormal cortico\u2010striatal synaptic plasticity contributes to abnormal reward\u2010learning behavior in patients with focal dystonia. Forty patients and 40 controls performed a reward gain and loss avoidance reversal learning task. Participant's behavior was fitted to a computational model of the basal ganglia incorporating detailed cortico\u2010striatal synaptic learning rules. Model comparisons were performed to assess the ability of four hypothesized receptor specific abnormalities of cortico\u2010striatal long\u2010term potentiation (\n                    <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>\n                    ) and long\u2010term depression (\n                    <jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>\n                    ): increased or decreased D1:\n                    <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>\n                    \/\n                    <jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>\n                    and increased or decreased D2:\n                    <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>\n                    \/\n                    <jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>\n                    to explain abnormal behavior in patients. Patients were selectively impaired in the post\u2010reversal phase of the reward task. Individual learning rates in the reward reversal task correlated with the severity of the patient's motor symptoms. A model of the striatum with decreased D2:\n                    <jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>\n                    \/\n                    <jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>\n                    best explained the patient's behavior, suggesting excessive D2 cortico\u2010striatal synaptic depotentiation could underpin biased reward\u2010learning in patients with cervical dystonia. Reversal learning impairment in cervical dystonia may be a behavioral correlate of D2\u2010specific abnormalities in cortico\u2010striatal synaptic plasticity. Reinforcement learning tasks with computational modeling could allow the identification of molecular targets for novel treatments based on their ability to restore normal reward\u2010learning behavior in these patients.\n                  <\/jats:p>","DOI":"10.1111\/ejn.14414","type":"journal-article","created":{"date-parts":[[2019,4,7]],"date-time":"2019-04-07T12:04:18Z","timestamp":1554638658000},"page":"3191-3204","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Maladaptive striatal plasticity and abnormal reward\u2010learning in cervical dystonia"],"prefix":"10.1111","volume":"50","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9866-1565","authenticated-orcid":false,"given":"Tom","family":"Gilbertson","sequence":"first","affiliation":[{"name":"Department of Neurology Ninewells Hospital &amp; Medical School Dundee UK"},{"name":"Division of Imaging Science and Technology Medical School University of Dundee Dundee UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Humphries","sequence":"additional","affiliation":[{"name":"Division of Neuroscience &amp; Experimental Psychology University of Manchester Manchester UK"},{"name":"School of Psychology University of Nottingham Nottingham UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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