Neonatal rotenone lesions cause onset of hyperactivity during juvenile and adulthood in the rat

Abstract Attention deficit hyperactivity disorder (ADHD) is characterized by behavioral and cognitive symptoms. Longitudinal studies demonstrated that the symptoms remains clinically significant for the majority of ADHD children into adulthood. Furthermore, a population-based birth cohort provided the initial evidence of adult ADHD that lacks a history of childhood ADHD. We previously demonstrated that neonatal exposure to bisphenol A, an environmental chemical caused hyperactivity in the juvenile. Here, we extend to examine other chemical such as rotenone, a dopaminergic toxins. Oral administration of rotenone (3 mg/kg) into 5-day-old male Wistar rats significantly caused hyperactivity at adulthood (8 ∼ 11 weeks old; p Thus, we demonstrate a rotenone models of ADHD whose onset varies during juvenile and adulthood.