Vldlr overexpression causes hyperactivity in rats.
Vldlr overexpression causes hyperactivity in rats.
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DOI：
10.1186/2040-2392-3-11
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发表时间：
2012-10-30
期刊：
影响因子：
6.2
通讯作者：
Mori N
中科院分区：
文献类型：
--
作者：
Iwata K;Izumo N;Matsuzaki H;Manabe T;Ishibashi Y;Ichitani Y;Yamada K;Thanseem I;Anitha A;Vasu MM;Shimmura C;Wakuda T;Kameno Y;Takahashi T;Iwata Y;Suzuki K;Nakamura K;Mori N
Reelin通过与脂蛋白受体Vldlr和Lrp 8结合来调节皮质脑结构中的神经元定位和神经元迁移。Reeler突变小鼠表现出严重的脑形态缺陷和行为异常。一些报道已经暗示了在神经发育和精神障碍的病因学中的reelin信号传导，包括自闭症、精神分裂症、双相情感障碍和抑郁症。此外，据报道，在自闭症患者死后的大脑中，VLDLR mRNA水平增加。我们产生过表达Vldlr的转基因（Tg）大鼠，并检查其组织学和行为学特征。自发运动活动显着增加Tg大鼠，没有检测到的脑组织学变化。此外，Tg大鼠在径向迷宫任务中倾向于表现出性能缺陷，这表明它们的空间工作记忆轻微受损。因此，Vldlr水平可能参与决定运动活性和记忆功能。与reeler小鼠不同，患有神经发育或精神疾病的患者没有表现出显著的神经解剖学畸变。因此，值得注意的是，从临床的角度来看，我们观察到Vldlr-Tg大鼠在神经解剖异常的情况下的行为表型。
Reelin regulates neuronal positioning in cortical brain structures and neuronal migration via binding to the lipoprotein receptors Vldlr and Lrp8. Reeler mutant mice display severe brain morphological defects and behavioral abnormalities. Several reports have implicated reelin signaling in the etiology of neurodevelopmental and psychiatric disorders, including autism, schizophrenia, bipolar disorder, and depression. Moreover, it has been reported that VLDLR mRNA levels are increased in the post-mortem brain of autistic patients. We generated transgenic (Tg) rats overexpressing Vldlr, and examined their histological and behavioral features. Spontaneous locomotor activity was significantly increased in Tg rats, without detectable changes in brain histology. Additionally, Tg rats tended to show performance deficits in the radial maze task, suggesting that their spatial working memory was slightly impaired. Thus, Vldlr levels may be involved in determining locomotor activity and memory function. Unlike reeler mice, patients with neurodevelopmental or psychiatric disorders do not show striking neuroanatomical aberrations. Therefore, it is notable, from a clinical point of view, that we observed behavioral phenotypes in Vldlr-Tg rats in the absence of neuroanatomical abnormalities.
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影响因子：
4.4
作者：
BAR, I;DEROUVROIT, CL;GOFFINET, AM
通讯作者：
GOFFINET, AM
影响因子：
16.2
作者：
Hiesberger, T;Trommsdorff, M;Herz, J
通讯作者：
Herz, J
影响因子：
16.2
作者：
OGAWA, M;MIYATA, T;MIKOSHIBA, K
通讯作者：
MIKOSHIBA, K
影响因子：
20.1
作者：
Masuzaki, H;Jingami, H;Nakao, K
通讯作者：
Nakao, K
影响因子：
5.3
作者：
Aguiló, A;Schwartz, TH;Yuste, R
通讯作者：
Yuste, R