{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:35:44Z","timestamp":1791300944806,"version":"4.1.0"},"reference-count":54,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,2,17]],"date-time":"2005-02-17T00:00:00Z","timestamp":1108598400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"MIUR-CNR"},{"name":"Ministero Salute"},{"DOI":"10.13039\/501100003407","name":"MIUR","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100003407","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2005,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long\u2010term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long\u2010lasting increase or an enduring decrease in synaptic strength, respectively referred to as long\u2010term potentiation (LTP), and long\u2010term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low\u2010frequency stimulation protocol, an active phenomenon defined \u201csynaptic depotentiation,\u201d required to erase redundant information. In the 6\u2010hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of <jats:sc>L<\/jats:sc>\u2010dopa\u2013treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and <jats:sc>L<\/jats:sc>\u2010dopa\u2013induced motor complications will be discussed. \u00a9 2005 Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.20394","type":"journal-article","created":{"date-parts":[[2005,2,17]],"date-time":"2005-02-17T18:40:45Z","timestamp":1108665645000},"page":"395-402","source":"Crossref","is-referenced-by-count":144,"title":["Striatal synaptic plasticity: Implications for motor learning and Parkinson's 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