Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice.

Journal: Translational psychiatry

Volume: 14

Issue: 1

Year of Publication: 2024

Affiliated Institutions:  Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan. d-mori@med.nagoya-u.ac.jp. Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan. Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University, Graduate School of Medicine, Nagoya, Japan. Department of Neuropharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan. Department of Pathophysiology of Mental Disorders, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan. Laboratory of Molecular Biology, Department of Bioscience, Graduate School of Life Sciences, Tokyo University of Agriculture, Tokyo, Japan. Department of Pathology of Mental Diseases, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan. Division of Cell Biology, International Center for Brain Science, Fujita Health University, - Dengakugakubo, Kusukake-cho, Toyoake, Aichi, Japan.

Abstract summary 

Whole genome analysis has identified rare copy number variations (CNV) that are strongly involved in the pathogenesis of psychiatric disorders, and 3q29 deletion has been found to have the largest effect size. The 3q29 deletion mice model (3q29-del mice) has been established as a good pathological model for schizophrenia based on phenotypic analysis; however, circadian rhythm and sleep, which are also closely related to neuropsychiatric disorders, have not been investigated. In this study, our aims were to reevaluate the pathogenesis of 3q29-del by recreating model mice and analyzing their behavior and to identify novel new insights into the temporal activity and temperature fluctuations of the mouse model using a recently developed small implantable accelerometer chip, Nano-tag. We generated 3q29-del mice using genome editing technology and reevaluated common behavioral phenotypes. We next implanted Nano-tag in the abdominal cavity of mice for continuous measurements of long-time activity and body temperature. Our model mice exhibited weight loss similar to that of other mice reported previously. A general behavioral battery test in the model mice revealed phenotypes similar to those observed in mouse models of schizophrenia, including increased rearing frequency. Intraperitoneal implantation of Nano-tag, a miniature acceleration sensor, resulted in hypersensitive and rapid increases in the activity and body temperature of 3q29-del mice upon switching to lights-off condition. Similar to the 3q29-del mice reported previously, these mice are a promising model animals for schizophrenia. Successive quantitative analysis may provide results that could help in treating sleep disorders closely associated with neuropsychiatric disorders.

Authors & Co-authors:  Mori Ikeda Sawahata Yamaguchi Kodama Hirao Arioka Okumura Inami Suzuki Hayashi Kato Nawa Miyata Kimura Kushima Aleksic Mizoguchi Nagai Nakazawa Hashimoto Kaibuchi Kume Yamada Ozaki

Study Outcome 

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Statistics
Citations :  McGuffin P, Owen MJ, Farmer AE. Genetic basis of schizophrenia. Lancet. 1995;346:678–82. doi: 10.1016/S0140-6736(95)92285-7.
Authors :  25
Identifiers
Doi : 138
SSN : 2158-3188
Study Population
Male,Female
Mesh Terms
Humans
Other Terms
Study Design
Study Approach
Quantitative
Country of Study
Publication Country
United States