title: Comprehensive behavioral analysis of RNG105 (Caprin1) heterozygous mice: Reduced social interaction and attenuated response to novelty.
abstract: RNG105 (also known as Caprin1) is a major RNA-binding protein in neuronal RNA granules, and is responsible for mRNA transport to dendrites and neuronal network formation. A recent study reported that a heterozygous mutation in the Rng105 gene was found in an autism spectrum disorder (ASD) patient, but it remains unclear whether there is a causal relation between RNG105 deficiency and ASD. Here, we subjected Rng105(+/-) mice to a comprehensive behavioral test battery, and revealed the influence of RNG105 deficiency on mouse behavior. Rng105(+/-) mice exhibited a reduced sociality in a home cage and a weak preference for social novelty. Consistently, the Rng105(+/-) mice also showed a weak preference for novel objects and novel place patterns. Furthermore, although the Rng105(+/-) mice exhibited normal memory acquisition, they tended to have relative difficulty in reversal learning in the spatial reference tasks. These findings suggest that the RNG105 heterozygous knockout leads to a reduction in sociality, response to novelty and flexibility in learning, which are implicated in ASD-like behavior.
authors: Laboratory of Neuronal Cell Biology, National Institute for Basic Biology, Okazaki, Aichi, Japan.|Department of Basic Biology, SOKENDAI, Okazaki, Aichi, Japan.
authors: Rie
authors: R
authors: Ohashi
authors: Section of Behavior Patterns, National Institute for Physical Science, Okazaki, Aichi, Japan.|Department of Physiology, SOKENDAI, Okazaki, Aichi, Japan.|Division of Animal Resources and Development, Life Science Research Center, University of Toyama, Toyama, Japan.
authors: Keizo
authors: K
authors: Takao
authors: Section of Behavior Patterns, National Institute for Physical Science, Okazaki, Aichi, Japan.|Division of Systems Medical Science, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake, Aichi, Japan.
authors: Tsuyoshi
authors: T
authors: Miyakawa
authors: Laboratory of Neuronal Cell Biology, National Institute for Basic Biology, Okazaki, Aichi, Japan.|Department of Basic Biology, SOKENDAI, Okazaki, Aichi, Japan.|Okazaki Institute for Integrative Bioscience, Okazaki, Aichi, Japan.
authors: Nobuyuki
authors: N
authors: Shiina
mesh_terms: D000818:Animals; D057565:Apathy; D000067877:Autism Spectrum Disorder / Q000235:genetics / Q000473:pathology / Q000523:psychology*; D001522:Behavior, Animal; D018797:Cell Cycle Proteins / Q000172:deficiency / Q000235:genetics*; D002531:Cerebellum / Q000378:metabolism / Q000473:pathology; D054022:Cerebrum / Q000378:metabolism / Q000473:pathology; D003594:Cytoplasmic Granules / Q000378:metabolism / Q000648:ultrastructure; D004195:Disease Models, Animal; D015870:Gene Expression; D006579:Heterozygote; D006801:Humans; D018782:Maze Learning; D008568:Memory; D051379:Mice; D009043:Motor Activity; D009154:Mutation; D009415:Nerve Net / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D034443:RNA Transport; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D012934:Social Isolation / Q000523:psychology*; D013647:Task Performance and Analysis
chemical_list: C486565:Caprin1 protein, mouse; D018797:Cell Cycle Proteins; D012333:RNA, Messenger