TY - JOUR
T1 - Comprehensive behavioral analysis of RNG105 (Caprin1) heterozygous mice
T2 - Reduced social interaction and attenuated response to novelty
AU - Ohashi, Rie
AU - Takao, Keizo
AU - Miyakawa, Tsuyoshi
AU - Shiina, Nobuyuki
N1 - Funding Information:
We thank C. Matsuda, Y. Koshidaka, A. Nakakihara, A. Imai, M. Ishikawa, N. Miyajima, S. Furukawa, M. Hyodo for technical assistance, and Dr. M. Tokunaga for providing Rng105+/− mice. This work was supported by the DAIKO Foundation (to NS) and a Grant-in-Aid for Scientific Research on Innovative Areas (Comprehensive Brain Science Network) from the Ministry of Education, Science, Sports and Culture of Japan.
PY - 2016/2/11
Y1 - 2016/2/11
N2 - 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.
AB - 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.
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U2 - 10.1038/srep20775
DO - 10.1038/srep20775
M3 - Article
C2 - 26865403
AN - SCOPUS:84958568947
SN - 2045-2322
VL - 6
JO - Scientific reports
JF - Scientific reports
M1 - 20775
ER -