{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T15:25:54Z","timestamp":1747149954505,"version":"3.40.5"},"reference-count":51,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:00:00Z","timestamp":1567987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Huntington's disease (HD) is a genetic neurodegenerative condition characterized by abnormal dopamine (DA)\u2013glutamate interactions, severe alterations in motor control, and reduced behavioral flexibility. Experimental models of disease show that during symptomatic phases, HD shares with other hyperkinetic disorders the loss of synaptic depotentiation in the striatal spiny projection neurons (SPNs). Here we test the hypothesis that corticostriatal long\u2010term depression (LTD), a well\u2010conserved synaptic scaling down response to environmental stimuli, is also altered in symptomatic male R6\/1 mice, a HD model with gradual development of symptoms. <jats:italic>In vitro<\/jats:italic> patch\u2010clamp and intracellular recordings of corticostriatal slices from R6\/1 mice confirm that, similar to other models characterized by hyperkinesia and striatal DA D1 receptor pathway dysregulation, once long\u2010term potentiation (LTP) is induced, synaptic depotentiation is lost. Our new observations show that activity\u2010dependent LTD was abolished in SPNs of mutant mice. In an experimental condition in which <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010aspartate (NMDA) receptors are normally not recruited, <jats:italic>in vitro<\/jats:italic> bath application of DA revealed an abnormal response of D1 receptors that caused a shift in synaptic plasticity direction resulting in an NMDA\u2010dependent LTP. Our results demonstrate that corticostriatal LTD is lost in R6\/1 mouse model and confirm the role of aberrant DA\u2013glutamate interactions in the alterations of synaptic scaling down associated with HD symptoms.<\/jats:p>","DOI":"10.1002\/jnr.24521","type":"journal-article","created":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T15:29:01Z","timestamp":1568042941000},"page":"1655-1664","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Corticostriatal synaptic plasticity alterations in the R6\/1 transgenic mouse model of Huntington's disease"],"prefix":"10.1002","volume":"97","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2885-8298","authenticated-orcid":false,"given":"Veronica","family":"Ghiglieri","sequence":"first","affiliation":[{"name":"Dipartimento di Filosofia, Scienze sociali, umane e della formazione Universit\u00e0 di Perugia Perugia Italy"},{"name":"Laboratorio di Neurofisiologia IRCCS Fondazione 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