Wrenn Craige C, Heitzer Andrew M, Roth Alexandra K, Nawrocki Lauren, Valdovinos Maria G
College of Pharmacy & Health Sciences, Drake University, 2507 University Avenue, Des Moines, IA 50311, USA.
Department of Psychology, Drake University, 2507 University Avenue, Des Moines, IA 50311, USA.
Neurosci Lett. 2015 Jan 12;585:109-13. doi: 10.1016/j.neulet.2014.11.035. Epub 2014 Nov 26.
Fragile X syndrome (FXS), a disorder caused by a mutation in the FMR1 gene, is often associated with Attention Deficit Hyperactivity Disorder (ADHD). Common treatments for the hyperactivity often seen in ADHD involve the use of stimulants and α2-adrenergic agonists. The Fmr1 knockout (KO) mouse has been found to be a valid model for FXS both biologically and behaviorally. Of particular interest to our research, the Fmr1 KO mouse has been demonstrated to show increased locomotion in comparison to wild type (WT) littermates. In the present study, we assessed the effects of clonidine (0.05 mg/kg) and methylphenidate (5 mg/kg) on motor activity in Fmr1 KO mice and their WT littermates in the open field test. Results showed that methylphenidate increased motor activity in both genotypes. Clonidine decreased motor activity in both genotypes, but the effect was delayed in the Fmr1 KO mice.
脆性X综合征(FXS)是一种由FMR1基因突变引起的疾病,常与注意力缺陷多动障碍(ADHD)相关。ADHD中常见的多动症状的常用治疗方法包括使用兴奋剂和α2-肾上腺素能激动剂。Fmr1基因敲除(KO)小鼠已被发现在生物学和行为学上都是FXS的有效模型。我们的研究特别感兴趣的是,与野生型(WT)同窝小鼠相比,Fmr1 KO小鼠已被证明表现出活动增加。在本研究中,我们在旷场试验中评估了可乐定(0.05 mg/kg)和哌甲酯(5 mg/kg)对Fmr1 KO小鼠及其WT同窝小鼠运动活动的影响。结果表明,哌甲酯增加了两种基因型小鼠的运动活动。可乐定降低了两种基因型小鼠的运动活动,但对Fmr1 KO小鼠的作用延迟。