PLoS ONE：研究多动症的新动物模型

多动症是儿童期最为常见的一种心理行为障碍，已引起了广大家长、老师、医务工作者及全社会的广泛关注。多动症呈慢性过程，症状持续多年，甚至终身存在。约70%的患儿症状会持续到青春期，30%的患儿症状会持续终身。近日，科学家开发出一种能更好研究多动症新的动物模型，这项研究发表在PLoS ONE期刊上。

OHSU和ONPRC科学家Jacob Raber等人研究发现老鼠携带某种突变基因会表现出类似人多动症的症状。科学家们认为这种独特的基因培育出的小鼠可以用来研究多动症。

在这项研究中，特定基因被称为SynCAM1，SynCAM1基因是在神经胶质细胞被发现的。神经胶质细胞也称神经胶质，是广泛分布于中枢神经系统内的，除了神经元以外的所有细胞。具有支持、滋养神经元的作用，也有吸收和调节某些活性物质的功能。胶质细胞虽有突起，但不具轴突，也不产生动作电位。

神经胶质细胞有分裂的能力，还能够吞噬因损伤而解体破碎的神经元，并能修补填充、形成瘢痕。大脑和小脑发育中细胞构筑的形成都有赖胶质细胞作前导，提供原初的框架结构。神经轴突再生过程必须有胶质细胞的导引才能成功。研究人员发现，老鼠携带显性/隐性基因形式是异常活跃的。在休息期间，小鼠表现出活动增强、活动更加频繁。此外，小鼠表现出焦虑程度下降，与确诊患有多动症的儿童相似。

ONPRC的资深科学家Ojeda表示：我们相信，这种动物模型可以更加真实地模仿多动症。（生物谷：Bioon.com）

doi:10.1371/journal.pone.0036424
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Astrocyte-Specific Disruption of SynCAM1 Signaling Results in ADHD-Like Behavioral Manifestations

Ursula S. Sandau¤, Zefora Alderman, Gabriel Corfas, Sergio R. Ojeda*, Jacob Raber*

SynCAM1 is an adhesion molecule involved in synaptic differentiation and organization. SynCAM1 is also expressed in astroglial cells where it mediates astrocyte-to astrocyte and glial-neuronal adhesive communication. In astrocytes, SynCAM1 is functionally linked to erbB4 receptors, which are involved in the control of both neuronal/glial development and mature neuronal and glial function. Here we report that mice carrying a dominant-negative form of SynCAM1 specifically targeted to astrocytes (termed GFAP-DNSynCAM1 mice) exhibit disrupted diurnal locomotor activity with enhanced and more frequent episodes of activity than control littermates during the day (when the animals are normally sleeping) accompanied by shorter periods of rest. GFAP-DNSynCAM1 mice also display high levels of basal activity in the dark period (the rodent's awake/active time) that are attenuated by the psychostimulant D,L-amphetamine, and reduced anxiety levels in response to both avoidable and unavoidable provoking stimuli. These results indicate that disruption of SynCAM1-dependent astroglial function results in behavioral abnormalities similar to those described in animals model of attention-deficit hyperactive disorder (ADHD), and suggest a hitherto unappreciated contribution of glial cells to the pathophysiology of this disorder.