<title_ja>神経ペプチド受容体VIPR2遺伝子のコピー数変異モデルマウスは超音波発声の変化と社会性行動の低下を示す</title_ja> <title_en>Altered ultrasonic vocalizations and impaired social behaviors in a mouse model of copy number variation in the neuropeptide receptor VIPR2 gene</title

2-B-P-104 <title_ja>神経ペプチド受容体VIPR2遺伝子のコピー数変異モデルマウスは超音波発声の変化と社会性行動の低下を示す</title_ja> <title_en>Altered ultrasonic vocalizations and impaired social behaviors in a mouse model of copy number variation in the neuropeptide receptor VIPR2 gene</title_en> 〇片平海雅¹、陳露¹、宮岡辰典¹、北川航平²、竹内修斗²、山田めゐ¹、金子皓¹、石本憲司¹、塚本智仁¹、樋野展正^1,3、中澤敬信⁴、橋本均^2,5,6,7,8、中川晋作¹、吾郷由希夫⁹ Kaiga Katahira¹, Lu Chen¹, Tatsunori Miyaoka¹, Kohei Kitagawa², Shuto Takeuchi², Mei Yamada¹, Zihao Jin¹, Kenji Ishimoto¹, Tomohito Tsukamoto¹, Nobumasa Hino^1,3, Takanobu Nakazawa⁴, Hitoshi Hashimoto^2,5,6,7,8, Shinsaku Nakagawa¹, Yukio Ago⁹ ¹大阪大・院薬・薬剤、²大阪大・院薬・神経薬理、³大阪大・感染症総合教育研究拠点、⁴東農大・生命科学・バイオサイエンス、⁵大阪大・院連合小児発達、⁶大阪大・データビリティフロンティア機構、⁷大阪大・先導的学際研究機構、⁸大阪大・院医・分子医薬、⁹広島大・院医（歯）・細胞分子薬理 ¹Lab Biopharmaceut, Grad Sch Pharmaceut Sci, Osaka Univ, ²Lab Mol Neuropharmacol, Grad Sch Pharmaceut Sci, Osaka Univ, ³CiDER, Osaka Univ, ⁴Dept Biosci, Grad Sch Life Sci, Tokyo Univ Agric, ⁵United Grad Sch Child Dev, Osaka Univ, ⁶Inst Datability Sci, Osaka Univ, ⁷Inst Open Transdiscip Res Initiatives, Osaka Univ, ⁸Dept Mol Pharmaceut Sci, Grad Sch Med, Osaka Univ, ⁹Dept Cell Mol Pharmacol, Grad Sch Biomed Health Sci, Hiroshima Univ Results of several large-scale genetic studies demonstrated that microduplications at 7q36.3, containing VIPR2 gene, represent risk factors for schizophrenia and autism spectrum disorder (ASD). VIPR2 encodes the VPAC2 receptor that binds two homologous neuropeptides, VIP and PACAP. To address how increased VIPR2 dosage might predispose to psychiatric disorders, we have developed a bacterial artificial chromosome (BAC) transgenic (Tg) mouse model of VIPR2 copy number variation. Here we investigated neonatal ultrasonic vocalizations (USVs), an early communicative signal of mother-pup interaction, and social behaviors in adults of VIPR2-BAC Tg mice. VIPR2 mRNA expression in the prefrontal cortex and hippocampus of VIPR2-BAC Tg mice was significantly increased compared to wild-type littermates. Toal and mean durations of USVs of VIPR2-BAC Tg pups at postnatal day 7 were significantly longer than those of wild-type pups. Additionally, qualitative analysis of USVs revealed that VIPR2-BAC Tg mice showed a low proportion of "short" calls. In adulthood, VIPR2-BAC Tg mice exhibited impaired social behaviors in the reciprocal social interaction test. These results suggest that increased VIPR2 disrupts social communication development and this might lead to form some features of ASD or schizophrenia.