| Abstract | Developmental dyslexia is the most common neurodevelopmental disorder and is thought to be very heterogeneous, as it is associated with both genetic and environmental factors and individuals with dyslexia may have deficits in one or multiple specific sub-deficits that each result in reading impairment, such as rapid auditory processing or prediction. Variation in DCDC2, a gene associated with dyslexia in humans, is associated with atypical development of reading related regions, including the cerebellum. Variation in this gene is associated with rapid auditory processing deficits in both humans and rodents, though prediction deficits are also likely as the cerebellum plays a role in forming predictions. We developed a novel Dcdc2 knockout rat model of dyslexia to determine whether variation in this gene is associated with deficits in rapid auditory processing and prediction capabilities. Using an extension of our rapid speech sound discrimination paradigm, we hypothesized that rats homozygous for the knockout would show impaired discrimination at increased speeds and an impaired ability to predict upcoming speech sounds, relative to wild-type and heterozygous rats. Counter to this hypothesis, variation in Dcdc2 was not associated with deficits in either rapid auditory processing or prediction, likely due to uniform dysregulation of neuronal migration in this global knockout model of Dcdc2. |
