Performance on a strategy set shifting task during adolescence in a genetic model of attention deficit/hyperactivity disorder: methylphenidate vs. atomoxetine treatments.

Performance on a strategy set shifting task during adolescence in a genetic model of attention deficit/hyperactivity disorder: methylphenidate vs. atomoxetine treatments.
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DOI:
10.1016/j.bbr.2013.01.027
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发表时间:
2013-05-01
影响因子:
2.7
通讯作者:
Kantak, Kathleen M.
Kantak, Kathleen M.
中科院分区:
心理学3区
文献类型:
--
作者:
Harvey, Roxann C.;Jordan, Chloe J.;Tassin, David H.;Moody, Kayla R.;Dwoskin, Linda P.;Kantak, Kathleen M.

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缺乏关于药物对注意力缺陷多动障碍(ADHD)青少年设置转换的影响的研究。ADHD的动物模型可能有助于探索这一差距。自发性高血压大鼠(SHR)是一种常用的ADHD动物模型。SHR和两个比较品系,Wistar-Kyoto(WKY)和Wistar(WIS),在青春期进行了评估,在一个策略集转移任务的条件下,0秒或15秒延迟到分娩。任务分为三个阶段:初始辨别、集合转移和反转学习。在0秒延迟下,SHR的表现与WKY和WIS一样好或更好。0.3 mg/kg/天托莫西汀给药几乎没有影响,除了在所有品系的集转换期间适度增加试验至标准外。在15秒延迟条件下,SHR组的杠杆按压反应时、标准延迟时间、实验遗漏次数均显著高于WKY组。1.5 mg/kg/天哌甲酯或0.3 mg/kg/天托莫西汀未系统性降低这些缺陷。在SHR的学习方面,哌甲酯改善了初始辨别力,而托莫西汀改善了组移,但破坏了初始辨别力。在逆转学习过程中,两种药物在SHR中均无效,托莫西汀使WKY的反应时间和试验遗漏更大。总的来说,WIS的表现与SHR或WKY不同,这取决于阶段。总的来说,青春期大鼠ADHD的遗传模型显示,哌甲酯和托莫西汀都不能减轻SHR在设定转换任务中的所有缺陷。因此,哌甲酯或托莫西汀单药治疗可能无法缓解ADHD青少年的所有集合转换任务相关缺陷。
Research examining medication effects on set shifting in teens with attention deficit/hyperactivity disorder (ADHD) is lacking. An animal model of ADHD may be useful for exploring this gap. The Spontaneously Hypertensive Rat (SHR) is a commonly used animal model of ADHD. SHR and two comparator strains, Wistar-Kyoto (WKY) and Wistar (WIS), were evaluated during adolescence in a strategy set shifting task under conditions of a 0-sec or 15-sec delay to reinforcer delivery. The task had three phases: initial discrimination, set shift and reversal learning. Under 0-sec delays, SHR performed as well as or better than WKY and WIS. Treatment with 0.3 mg/kg/day atomoxetine had little effect, other than to modestly increase trials to criterion during set shifting in all strains. Under 15-sec delays, SHR had longer lever press reaction times, longer latencies to criterion and more trial omissions than WKY during set shifting and reversal learning. These deficits were not reduced systematically by 1.5 mg/kg/day methylphenidate or 0.3 mg/kg/day atomoxetine. Regarding learning in SHR, methylphenidate improved initial discrimination, whereas atomoxetine improved set shifting but disrupted initial discrimination. During reversal learning, both drugs were ineffective in SHR, and atomoxetine made reaction time and trial omissions greater in WKY. Overall, WIS performance differed from SHR or WKY, depending on phase. Collectively, a genetic model of ADHD in adolescent rats revealed that neither methylphenidate nor atomoxetine mitigated all deficits in SHR during the set shifting task. Thus, methylphenidate or atomoxetine monotherapy may not mitigate all set shift task-related deficits in teens with ADHD.
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