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dc.contributor.authorNagode, D.A.
dc.contributor.authorMeng, X.
dc.contributor.authorWinkowski, D.E.
dc.date.accessioned2019-07-15T16:17:01Z
dc.date.available2019-07-15T16:17:01Z
dc.date.issued2017
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85011692257&doi=10.1016%2fj.celrep.2017.01.006&partnerID=40&md5=c37e5d4b26bd61a212b70fb714a4bfc8
dc.identifier.urihttp://hdl.handle.net/10713/10059
dc.description.abstractAutism spectrum disorder (ASD) involves deficits in speech and sound processing. Cortical circuit changes during early development likely contribute to such deficits. Subplate neurons (SPNs) form the earliest cortical microcircuits and are required for normal development of thalamocortical and intracortical circuits. Prenatal valproic acid (VPA) increases ASD risk, especially when present during a critical time window coinciding with SPN genesis. Using optical circuit mapping in mouse auditory cortex, we find that VPA exposure on E12 altered the functional excitatory and inhibitory connectivity of SPNs. Circuit changes manifested as “patches” of mostly increased connection probability or strength in the first postnatal week and as general hyper-connectivity after P10, shortly after ear opening. These results suggest that prenatal VPA exposure severely affects the developmental trajectory of cortical circuits and that sensory-driven activity may exacerbate earlier, subtle connectivity deficits. Our findings identify the subplate as a possible common pathophysiological substrate of deficits in ASD. Copyright 2017 The Author(s)en_US
dc.description.urihttps://www.doi.org/10.1016/j.celrep.2017.01.006en_US
dc.language.isoen_USen_US
dc.publisherElsevier B.V.en_US
dc.relation.ispartofCell Reports
dc.subjectautismen_US
dc.subjectcortexen_US
dc.subjectdevelopmenten_US
dc.subjectsubplateen_US
dc.subjectvalproateen_US
dc.titleAbnormal Development of the Earliest Cortical Circuits in a Mouse Model of Autism Spectrum Disorderen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.celrep.2017.01.006
dc.identifier.pmid28147267


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