{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T07:14:08Z","timestamp":1790061248963,"version":"4.0.1"},"reference-count":88,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T00:00:00Z","timestamp":1778198400000},"content-version":"vor","delay-in-days":127,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100012138","name":"Nellie Ball Collaborative","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100012138","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Iowa Neuroscience Institute Carver Trust Schizophrenia Research Program of Excellence"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>16p11.2 microduplication (16p11.2dp\/+) is associated with neuropsychiatric disorders including schizophrenia, autism and intellectual disability. Cerebellar abnormalities have been implicated in these disorders. In 16p11.2dp\/+ mice, the cerebellum displays significant transcriptional dysregulation, and humans with 16p11.2 microduplication have decreased cerebellar volume. Despite this, cerebellar anatomy and cerebellar-dependent behaviour in 16p11.2dp\/+ mice remain uncharacterized. To address this, we histologically examined the cerebellar cortex in 16p11.2dp\/+ mice. There were no structural differences in cerebellar lobule IV\/V or impairments in gait or motor coordination, commonly associated with lobule IV\/V. In contrast, more Purkinje cells (PCs) were mislocalized to the granule layer and parvalbumin expression was decreased in molecular layer interneurons (MLIs) in cerebellar lobule VI of 16p11.2dp\/+ mice, but not in lobule IV\/V. Cerebellar lobule VI is associated with delay eyeblink conditioning, and 16p11.2dp\/+ mice are impaired in cerebellum-dependent associative learning on this task. Specifically, 16p11.2dp\/+ mice had conditioned response (CR) percentage and CR onset latency deficits, suggesting lobule-specific alterations to PC localization and MLI parvalbumin expression may impair learning and adaptive timing of cerebellar-driven CRs. Similarly, schizophrenia involves CR acquisition deficits in delay eyeblink conditioning. Further investigation of the cerebellum in 16p11.2dp\/+ mice may provide insights into the pathogenesis of neuropsychiatric disorders linked to this copy number variant.<\/jats:p>","DOI":"10.1093\/braincomms\/fcag156","type":"journal-article","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T11:38:33Z","timestamp":1778153913000},"source":"Crossref","is-referenced-by-count":1,"title":["Cerebellar structure and function abnormalities in 16p11.2 microduplication mice"],"prefix":"10.1093","volume":"8","author":[{"given":"Cessily","family":"Hayes","sequence":"first","affiliation":[{"name":"Iowa Neuroscience Institute, University of Iowa , Iowa City, IA 52242 ,","place":["USA"]},{"name":"Department of Psychiatry, Carver College of Medicine, University of Iowa , Iowa City, IA 52242 ,","place":["USA"]},{"name":"Pharmaceutical Sciences and Experimental Therapeutics, College of Pharmacy, University of Iowa , Iowa City, IA 52242 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