title: 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 (3mg/kg) into 5-day-old male Wistar rats significantly caused hyperactivity at adulthood (8∼11 weeks old; p<0.05). It was about 1.3∼1.4-fold more active in the nocturnal phase after administration of rotenone than control rats. Higher dose (16mg/kg) or repeated lower dose of rotenone (1mg/kg/day for 4days) caused hyperactivity in the juvenile. Furthermore, DNA array analyses showed that neonatal exposure to rotenone altered the levels of gene expression of several molecules related to apoptosis/cell cycle, ATPase, skeletal molecule, and glioma. Bivariate normal distribution analysis indicates no correlation in gene expression between a hyperactivity disorder model and a Parkinson's disease model by rotenone. Thus, we demonstrate a rotenone models of ADHD whose onset varies during juvenile and adulthood.
authors.affiliation: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506, Japan. Electronic address: ishidou@nies.go.jp.
authors.forename: Masami
authors.initials: M
authors.lastname: Ishido
authors.affiliation: Center for Health and Environmental Risk Research, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba 305-8506, Japan.
authors.forename: Junko
authors.initials: J
authors.lastname: Suzuki
authors.affiliation: Facul. Of Science, Toho University, Funabashi, 274-8510, Japan.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Masuo
mesh_terms: D017109:Akathisia, Drug-Induced / Q000473:pathology*; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000187:drug effects / Q000473:pathology; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects*; D008297:Male; D009043:Motor Activity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017208:Rats, Wistar; D012402:Rotenone / Q000633:toxicity*; D013378:Substantia Nigra / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism
chemical_list: D012402:Rotenone
keywords: Dopaminergic neuron; Hyperactivity disorder; Rotenone; Transcriptome