IL1RAPL1 knockout mice show spine density decrease, learning deficiency, hyperactivity and reduced anxiety-like behaviours

Misato Yasumura, Tomoyuki Yoshida, Maya Yamazaki, Manabu Abe, Rie Natsume, Kouta Kanno, Takeshi Uemura, Keizo Takao, Kenji Sakimura, Takefumi Kikusui, Tsuyoshi Miyakawa, Masayoshi Mishina

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Abstract

IL-1 receptor accessory protein-like 1 (IL1RAPL1) is responsible for nonsyndromic intellectual disability and is associated with autism. IL1RAPL1 mediates excitatory synapse formation through trans-synaptic interaction with PTPd. Here, we showed that the spine density of cortical neurons was significantly reduced in IL1RAPL1 knockout mice. The spatial reference and working memories and remote fear memory were mildly impaired in IL1RAPL1 knockout mice. Furthermore, the behavioural flexibility was slightly reduced in the T-maze test. Interestingly, the performance of IL1RAPL1 knockout mice in the rotarod test was significantly better than that of wild-type mice. Moreover, IL1RAPL1 knockout mice consistently exhibited high locomotor activity in all the tasks examined. In addition, open-space and height anxiety-like behaviours were decreased in IL1RAPL1 knockout mice. These results suggest that IL1RAPL1 ablation resulted in spine density decrease and affected not only learning but also behavioural flexibility, locomotor activity and anxiety.

Original languageEnglish
Article number6613
JournalScientific reports
Volume4
DOIs
Publication statusPublished - 14-10-2014

All Science Journal Classification (ASJC) codes

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    Yasumura, M., Yoshida, T., Yamazaki, M., Abe, M., Natsume, R., Kanno, K., Uemura, T., Takao, K., Sakimura, K., Kikusui, T., Miyakawa, T., & Mishina, M. (2014). IL1RAPL1 knockout mice show spine density decrease, learning deficiency, hyperactivity and reduced anxiety-like behaviours. Scientific reports, 4, [6613]. https://doi.org/10.1038/srep06613