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注意缺陷多动障碍的动物模型。

Animal models of attention-deficit/hyperactivity disorder.

机构信息

Department of Biological Psychiatry, Graduate School of Medicine, Tohoku University, Japan.

出版信息

Biol Pharm Bull. 2011;34(9):1373-6. doi: 10.1248/bpb.34.1373.

Abstract

Attention-deficit hyperactivity disorder (AD/HD) is a clinically heterogenous disorder including hyperactivity, impulsivity, and inattention. Both psychostimulant and non-psychostimulant drugs such as methylphenidate and atomoxetine, respectively, to modulate catecholeamine neurotransmission are used as current pharmacotherapies for AD/HD. Multiple lines of evidence suggest that genetic factors play major roles in the etiology of AD/HD. meta-Analyses and pooled data analyses have suggested associations between AD/HD and polymorphisms in genes encoding monoamine neurotransmission molecules. There has been considerable research on this disorder using genetic, pharmacological, and neuroimaging approaches, and several animal models of AD/HD such as spontaneously hypertensive rat (SHR), dopamine transporter (DAT) knockout mice, coloboma mutant mouse, and Grin1 mutant mouse have been reported. These animal models are valuable tools for investigating molecular, cellular, and behavioral mechanisms as well as the neural development and circuit mechanisms of AD/HD. Here, we review the recent literature on animal models of AD/HD and discuss their advantages and limitations.

摘要

注意缺陷多动障碍(AD/HD)是一种临床表现异质性的疾病,包括多动、冲动和注意力不集中。目前,AD/HD 的药物治疗主要采用哌甲酯和托莫西汀等调节儿茶酚胺递质的精神兴奋剂和非精神兴奋剂药物。多项证据表明,遗传因素在 AD/HD 的发病机制中起主要作用。荟萃分析和汇总数据分析表明,AD/HD 与编码单胺递质分子的基因多态性之间存在关联。通过遗传、药理学和神经影像学方法对这种疾病进行了大量研究,并且已经报道了几种 AD/HD 的动物模型,例如自发性高血压大鼠(SHR)、多巴胺转运蛋白(DAT)敲除小鼠、脉络膜裂畸形突变小鼠和 Grin1 突变小鼠。这些动物模型是研究 AD/HD 的分子、细胞和行为机制以及神经发育和回路机制的有价值的工具。在这里,我们回顾了 AD/HD 动物模型的最新文献,并讨论了它们的优缺点。

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