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The expression levels of <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>s and immune localization of the <jats:styled-content style=\"fixed-case\">NT<\/jats:styled-content>\u20103 protein and its receptor TrkC are altered in the striatum following damage induced by an in vivo treatment with 3\u2010nitropropionic acid (3\u2010<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>), a mitochondrial toxin used to mimic the histopathological hallmarks of Huntington's disease (<jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>). The aim of this study was to evaluate the role of <jats:styled-content style=\"fixed-case\">NT<\/jats:styled-content>\u20103 on corticostriatal synaptic transmission and its plasticity in both the control and damaged striatum.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Corticostriatal population spikes were electrophysiologically recorded and striatal synaptic plasticity was induced by high\u2010frequency stimulation. Further, the phosphorylation status of Trk receptors was tested under conditions that imitated electrophysiological experiments.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">NT<\/jats:styled-content>\u20103 modulates both synaptic transmission and plasticity in the striatum; nonetheless, synaptic plasticity was modified by the 3\u2010<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content> treatment, where instead of producing striatal long\u2010term depression (<jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>), long\u2010term potentiation (<jats:styled-content style=\"fixed-case\">LTP<\/jats:styled-content>) was obtained. Moreover, the administration of <jats:styled-content style=\"fixed-case\">NT<\/jats:styled-content>\u20103 in the recording bath restored the plasticity observed under control conditions (<jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content>) in this model of striatal degeneration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">NT<\/jats:styled-content>\u20103 modulates corticostriatal transmission through TrkB stimulation and restores striatal <jats:styled-content style=\"fixed-case\">LTD<\/jats:styled-content> by signaling through its TrkC receptor.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12824","type":"journal-article","created":{"date-parts":[[2018,2,17]],"date-time":"2018-02-17T18:18:40Z","timestamp":1518891520000},"page":"353-363","source":"Crossref","is-referenced-by-count":30,"title":["Neurotrophin\u20103 restores synaptic plasticity in the striatum of a mouse model of Huntington's 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en Biomedicina Universidad Nacional Aut\u00f3noma de M\u00e9xico FES Iztacala  Tlalnepantla M\u00e9xico"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2910-9248","authenticated-orcid":false,"given":"Elizabeth","family":"Hern\u00e1ndez\u2010Echeagaray","sequence":"additional","affiliation":[{"name":"Laboratorio de neurofisiolog\u00eda del desarrollo y la neurodegeneraci\u00f3n Unidad de Investigaci\u00f3n en Biomedicina Universidad Nacional Aut\u00f3noma de M\u00e9xico FES Iztacala  Tlalnepantla 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