Transcriptional profiling of SHR/NCrl prefrontal cortex shows hyperactivity‐associated genes responsive to amphetamine challenge

摘要: Several studies suggest a strong genetic component of attention-deficit/hyperactivity disorder (ADHD), complex neurodevelopmental characterized by inappropriate levels hyperactivity, impulsivity and inattention. Determining specific risk variants for each symptom dimension ADHD may aid in the identification biological factors disorder. In this study, we explored potential underpinnings hyperactive phenotype ADHD. To end, examined differentially expressed genes (DEGs) prefrontal cortex (PFC) SHR/NCrl, an animal model ADHD, compared with its control, Wistar Kyoto (WKY/NCrl) rat rat, strain used to represent 'normal' heterogeneous population. Relative WKY/NCrl controls, SHR/NCrl showed hyperactivity open-field test. Treatment drug, amphetamine (AMPH) reduced SHR/NCrl. Meanwhile, AMPH increased locomotor activity rats. Gene expression analysis found 21 common upregulated 36 downregulated PFC drug-naive when Of these DEGs, two genes, Atxn7 Per2, which are involved transcription circadian rhythm, respectively, were following treatment Quantitative real-time-polymerase chain reaction analyses verified patterns AMPH-treated The present findings indicate that be associated Further warranted establish roles Per2 mediating hyperactivity.