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Vldlr overexpression causes hyperactivity in rats

Author(s): Iwata Keiko | Izumo Nobuo | Matsuzaki Hideo | Manabe Takayuki | Ishibashi Yukiko | Ichitani Yukio | Yamada Kazuo | Thanseem Ismail | Anitha Ayyappan | Vasu Mahesh | Shimmura Chie | Wakuda Tomoyasu | Kameno Yosuke | Takahashi Taro | Iwata Yasuhide | Suzuki Katsuaki | Nakamura Kazuhiko | Mori Norio

Journal: Molecular Autism
ISSN 2040-2392

Volume: 3;
Issue: 1;
Start page: 11;
Date: 2012;
Original page

Keywords: Hyperactivity | Neurodevelopmental disorder | Psychiatric disorder | Reelin | Transgenic rat | Vldlr

Abstract Background 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. Methods We generated transgenic (Tg) rats overexpressing Vldlr, and examined their histological and behavioral features. Results 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. Conclusions 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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