Psychiatric-disorder-related behavioral phenotypes and cortical hyperactivity in a mouse model of 3q29 deletion syndrome

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  • Baba Masayuki
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Yokoyama Kazumasa
    Pharmaceut. Res. Div., Takeda Pharmaceut. Co. Ltd.
  • Seiriki Kaoru
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. Interdiscip. Program Biomed. Sci., Inst. Transdiscip. Grad. Degree Program, Osaka Univ.
  • Matsumura Kensuke
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. Interdiscip. Program Biomed. Sci., Inst. Transdiscip. Grad. Degree Program, Osaka Univ. JSPS
  • Kondo Momoka
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Yamamoto Kana
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Kasai Atsushi
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Ago Yukio
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. Lab. Biopharmaceutics, Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Nagayasu Kazuki
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ.
  • Hayata Atsuko
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. United Grad. Sch. Child Dev., Osaka Univ.
  • Yamaguchi Shun
    Dept. Morphological Neurosci., Gifu Univ. Grad. Sch. Med. Ctr. Highly Adv. Integration Nano Life Sci., Gifu Univ.
  • Mori Daisuke
    Dept. Psychiatry, Nagoya Univ. Grad. Sch. Med. Brain Mind Res. Ctr., Nagoya Univ.
  • Ozaki Norio
    Dept. Psychiatry, Nagoya Univ. Grad. Sch. Med.
  • Yamamoto Tadashi
    Lab. IImmunogenetics, Ctr. Integr. Med. Sci., RIKEN Cell Signal Unit, Okinawa Inst. Sci. Tech. Grad. Univ.
  • Takuma Kazuhiro
    United Grad. Sch. Child Dev., Osaka Univ. Dept. Pharmacol., Grad. Sch. Dent., Osaka Univ.
  • Hashimoto Ryota
    Dept. Pathol. Mental Diseases, Natl. Inst. Mental Health, Natl. Ctr. Neurology Psychiatry Osaka Univ.
  • Hashimoto Hitoshi
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. United Grad. Sch. Child Dev., Osaka Univ.
  • Nakazawa Takanobu
    Lab. Mol. Neuropharmacol., Grad. Sch. Pharmaceut. Sci., Osaka Univ. Dept. Pharmacol., Grad. Sch. Dent., Osaka Univ.

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Other Title
  • ３ｑ２９欠失症候群モデルマウスにおける精神疾患様の行動異常と大脳皮質神経細胞の過活動

Abstract

<p>The 3q29 microdeletion is a rare recurrent copy number variant (CNV) leading to an increased risk for neurodevelopmental disorders, such as intellectual disability and autism spectrum disorder (ASD), and a &gt;40-fold increased risk for schizophrenia. However, the neurobiological basis for 3q29 deletion syndrome is currently unknown. In order to investigate the biological changes induced by the microdeletion, we generated a mouse model of human 3q29 deletion syndrome by deleting the orthologous region. 3q29 deletion (Df/+) mice showed reduced body and brain weight. Importantly, Df/+ mice showed deficits in social interaction and prepulse inhibition, which are reminiscent of the phenotypes in patients with 3q29 deletion syndrome. By unbiasedly analyzing the whole-brain neural activity, we found that neuronal activity was abnormally activated in a restricted region of the cortex of Df/+ mice. Furthermore, we found that the expression levels of immediate early genes were increased and that the number of parvalbumin positive neurons was decreased in the cortex of Df/+ mice. Our results suggest that Df/+ mice may provide important clues for understanding the disease-causative molecular and cellular pathology of psychiatric disorders.</p>

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