Journal
SCIENTIFIC REPORTS
Volume 4, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/srep06613
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Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan [24249014, 22123008, 221S0003]
- Japan Society for the Promotion of Science (JSPS)
- Grants-in-Aid for Scientific Research [25830048, 13J02670, 25118007, 25350989, 25242078, 23248049, 25116526, 22123008, 26350979, 26115529] Funding Source: KAKEN
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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 PTP delta. 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.
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