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

Research output: Contribution to journalArticle

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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

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Interleukin-1 Receptors
Knockout Mice
Spine
Anxiety
Learning
Proteins
Locomotion
Rotarod Performance Test
Long-Term Memory
Autistic Disorder
Short-Term Memory
Intellectual Disability
Synapses
Fear
Neurons

All Science Journal Classification (ASJC) codes

  • General

Cite this

Yasumura, Misato ; Yoshida, Tomoyuki ; Yamazaki, Maya ; Abe, Manabu ; Natsume, Rie ; Kanno, Kouta ; Uemura, Takeshi ; Takao, Keizo ; Sakimura, Kenji ; Kikusui, Takefumi ; Miyakawa, Tsuyoshi ; Mishina, Masayoshi. / IL1RAPL1 knockout mice show spine density decrease, learning deficiency, hyperactivity and reduced anxiety-like behaviours. In: Scientific reports. 2014 ; Vol. 4.
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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.",
author = "Misato Yasumura and Tomoyuki Yoshida and Maya Yamazaki and Manabu Abe and Rie Natsume and Kouta Kanno and Takeshi Uemura and Keizo Takao and Kenji Sakimura and Takefumi Kikusui and Tsuyoshi Miyakawa and Masayoshi Mishina",
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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, vol. 4, 6613. https://doi.org/10.1038/srep06613

IL1RAPL1 knockout mice show spine density decrease, learning deficiency, hyperactivity and reduced anxiety-like behaviours. / Yasumura, Misato; Yoshida, Tomoyuki; Yamazaki, Maya; Abe, Manabu; Natsume, Rie; Kanno, Kouta; Uemura, Takeshi; Takao, Keizo; Sakimura, Kenji; Kikusui, Takefumi; Miyakawa, Tsuyoshi; Mishina, Masayoshi.

In: Scientific reports, Vol. 4, 6613, 14.10.2014.

Research output: Contribution to journalArticle

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AU - Yasumura, Misato

AU - Yoshida, Tomoyuki

AU - Yamazaki, Maya

AU - Abe, Manabu

AU - Natsume, Rie

AU - Kanno, Kouta

AU - Uemura, Takeshi

AU - Takao, Keizo

AU - Sakimura, Kenji

AU - Kikusui, Takefumi

AU - Miyakawa, Tsuyoshi

AU - Mishina, Masayoshi

PY - 2014/10/14

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N2 - 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.

AB - 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.

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