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Striosomal and matrix compartments receive inputs from limbic system\u2010related and sensorimotor cortices, respectively. Here, we investigate the impact on the corticostriosomal pathway in the valproic acid (VPA)\u2010induced autism spectrum disorder mouse model. VPA administration during the neurogenesis time windows of striosomes, but not the matrix, resulted in aberrant compartmentation [\n                    <jats:italic>i.e.<\/jats:italic>\n                    , maternal VPA injections at embryonic day (E)12.75 decreased \u03bc\u2010opioid receptor\u2013positive striosomes, but increased calbindin\u2010positive matrix in the rostral striatum]. VPA\n                    <jats:sup>E12.75<\/jats:sup>\n                    treatment also impaired the aggregation of cells pulse labeled with 5\u2010bromo\u20102\u2032\u2010deoxyuridine at E12.75 into striosomal cell clusters, which suggests defective segregation of striosomal cells from matrix cells. This possibility was supported by our findings that VPA\n                    <jats:sup>E12.75<\/jats:sup>\n                    treatment altered the expression of ephrinA5 and EphA4, two molecules that are related to compartmental segregation. In the VPA\n                    <jats:sup>E12.75<\/jats:sup>\n                    neocortex, Foxp2\u2010positive neurons were decreased in layer VI, but increased in layer V, which projects to the striosomal compartment. We also investigated VPA effects on the corticostriosomal pathway. VPA\n                    <jats:sup>E12.75<\/jats:sup>\n                    treatment decreased the putative corticostriosomal synapses of striosomal neurons and induced an aberrant pattern of isolation stress\u2013induced ultrasonic vocalizations. Of interest, risperidone treatments conjointly improved ultrasonic vocalizations and restored the striosomal compartment in VPA\n                    <jats:sup>E12.75<\/jats:sup>\n                    pups. Collectively, dysfunctional corticostriatal pathways, particularly\n                    <jats:italic>via<\/jats:italic>\n                    the aberrant striosomal compartment, may be involved in autism spectrum disorder pathophysiology.\u2014Kuo, H.\u2010Y., Liu, F.\u2010C. Valproic acid induces aberrant development of striatal compartments and corticostriatal pathways in a mouse model of autism spectrum disorder. FASEB J. 31, 4458\u20134471 (2017).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201700054r","type":"journal-article","created":{"date-parts":[[2017,7,7]],"date-time":"2017-07-07T20:10:17Z","timestamp":1499458217000},"page":"4458-4471","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Valproic acid induces aberrant development of striatal compartments and corticostriatal pathways in a mouse model of autism spectrum disorder"],"prefix":"10.1096","volume":"31","author":[{"given":"Hsiao\u2010Ying","family":"Kuo","sequence":"first","affiliation":[{"name":"Institute of Neuroscience National Yang\u2010Ming University Taipei Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fu\u2010Chin","family":"Liu","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience National Yang\u2010Ming University Taipei 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