| dc.description.abstract | Dyslexia is a prevalent developmental disorder characterized by unexpected reading difficulty in children and adults with otherwise normal nonverbal IQ. Dyslexia is a heterogeneous disorder and a variety of deficits are observed in the population, with auditory perception and rapid stimulus processing deficits occurring most frequently, though not always in the same individuals (Ferrer et al., 2009; Peterson & Pennington, 2012, Shaywitz, 1998). Genetic variants are likely related to this heterogeneity. One such gene that has been reliably linked to dyslexia is the neural migration gene DCDC2 (Galaburda et al., 2006; Neef et al., 2017, Scerri et al., 2011). Suppression of this gene in a rat model dramatically impairs speech-sound discrimination ability from a stream of rapidly-presented auditory stimuli (Centanni et al., 2016), suggesting a potential role for this gene in rapid stimulus processing deficits in humans and supporting a prior study linking this gene to reading speed (Neef et al., 2017). One potential casualty of processing speed impairments is the ability to process unpredictable stimuli. In the current study, we designed a rapid speech sound discrimination and prediction task to evaluate whether the rapid speech sound impairment previously linked with Dcdc2 also causes deficits on a prediction task. If increased presentation rate impairs the ability to process unpredictable stimuli, then the addition of a stable predictor sound should improve performance. To test this hypothesis, homozygous Dcdc2-knockout, heterozygous Dcdc2-knockout, and wild type rats were trained to respond to a target sound /dad/ in a stream of rapidly presented distractors in the presence or absence of a predictor sound /bad/, which occurred reliably prior to the target in 40% of trials. In wild type rats, the results indicate the presence of a predictor enhances response to the target /dad/ at low speeds, but as the stimulus presentation rate increased the rats began responding to the predictor /bad/ rather than the target. I will present these findings as well as pilot data from rats with Dcdc2 knockout to investigate the role of this gene on the response to a stable predictor. | |
