{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T02:25:13Z","timestamp":1778725513230,"version":"3.51.4"},"reference-count":75,"publisher":"Society for Neuroscience","issue":"17","license":[{"start":{"date-parts":[[2016,10,27]],"date-time":"2016-10-27T00:00:00Z","timestamp":1477526400000},"content-version":"vor","delay-in-days":183,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2016,4,27]]},"abstract":"<jats:p>Dyslexia is the most common developmental language disorder and is marked by deficits in reading and phonological awareness. One theory of dyslexia suggests that the phonological awareness deficit is due to abnormal auditory processing of speech sounds. Variants in<jats:italic>DCDC2<\/jats:italic>and several other neural migration genes are associated with dyslexia and may contribute to auditory processing deficits. In the current study, we tested the hypothesis that RNAi suppression of<jats:italic>Dcdc2<\/jats:italic>in rats causes abnormal cortical responses to sound and impaired speech sound discrimination. In the current study, rats were subjected<jats:italic>in utero<\/jats:italic>to RNA interference targeting of the gene<jats:italic>Dcdc2<\/jats:italic>or a scrambled sequence. Primary auditory cortex (A1) responses were acquired from 11 rats (5 with<jats:italic>Dcdc2<\/jats:italic>RNAi; DC\u2212) before any behavioral training. A separate group of 8 rats (3 DC\u2212) were trained on a variety of speech sound discrimination tasks, and auditory cortex responses were acquired following training.<jats:italic>Dcdc2<\/jats:italic>RNAi nearly eliminated the ability of rats to identify specific speech sounds from a continuous train of speech sounds but did not impair performance during discrimination of isolated speech sounds. The neural responses to speech sounds in A1 were not degraded as a function of presentation rate before training. These results suggest that A1 is not directly involved in the impaired speech discrimination caused by<jats:italic>Dcdc2<\/jats:italic>RNAi. This result contrasts earlier results using<jats:italic>Kiaa0319<\/jats:italic>RNAi and suggests that different dyslexia genes may cause different deficits in the speech processing circuitry, which may explain differential responses to therapy.<\/jats:p><jats:p><jats:bold>SIGNIFICANCE STATEMENT<\/jats:bold>Although dyslexia is diagnosed through reading difficulty, there is a great deal of variation in the phenotypes of these individuals. The underlying neural and genetic mechanisms causing these differences are still widely debated. In the current study, we demonstrate that suppression of a candidate-dyslexia gene causes deficits on tasks of rapid stimulus processing. These animals also exhibited abnormal neural plasticity after training, which may be a mechanism for why some children with dyslexia do not respond to intervention. These results are in stark contrast to our previous work with a different candidate gene, which caused a different set of deficits. Our results shed some light on possible neural and genetic mechanisms causing heterogeneity in the dyslexic population.<\/jats:p>","DOI":"10.1523\/jneurosci.4202-15.2016","type":"journal-article","created":{"date-parts":[[2016,4,27]],"date-time":"2016-04-27T16:52:38Z","timestamp":1461775958000},"page":"4895-4906","source":"Crossref","is-referenced-by-count":37,"title":["Knockdown of Dyslexia-Gene<i>Dcdc2<\/i>Interferes with Speech Sound Discrimination in Continuous Streams"],"prefix":"10.1523","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9889-334X","authenticated-orcid":false,"given":"Tracy Michelle","family":"Centanni","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne 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