| 研究課題/領域番号 |
20F20704
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| 研究種目 |
特別研究員奨励費
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| 配分区分 | 補助金 |
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| 応募区分 | 外国 |
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| 審査区分 |
小区分48020:生理学関連
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| 研究機関 | 神戸大学 |
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研究代表者 |
内匠 透 (2020) 神戸大学, 医学研究科, 教授 (00222092)
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| 研究分担者 |
BALASURIYA BALASURIYA 神戸大学, 医学研究科, 外国人特別研究員
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| 受入研究者 |
内匠 透 (2021-2022) 神戸大学, 医学研究科, 教授 (00222092)
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| 外国人特別研究員 |
BALASURIYA BALASURIYA 神戸大学, 医学(系)研究科(研究院), 外国人特別研究員
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| 研究期間 (年度) |
2020-11-13 – 2023-03-31
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| 研究課題ステータス |
完了 (2022年度)
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| 配分額 *注記 |
2,300千円 (直接経費: 2,300千円)
2022年度: 1,100千円 (直接経費: 1,100千円)
2021年度: 900千円 (直接経費: 900千円)
2020年度: 300千円 (直接経費: 300千円)
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| キーワード | autism / intestine |
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| 研究開始時の研究の概要 |
Autism is a highly prevalent neurological disorder characterized by impaired social interactions and stereotyped or repetitive behaviours. Autism-associated GI symptoms frequently present from early childhood to adulthood and patients with autism are approximately four-fold more likely to be hospitalized with GI disorders. GI function is regulated by the intrinsic enteric nervous system (ENS). We characterize the GI phenotype in mouse models of autism in order to identify therapeutic targets to treat GI dysfunction.
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| 研究実績の概要 |
Chromosome 15q duplication Syndrome is a neurodevelopmental disorder. Approximately 80% of individuals with 15q duplications (15q dup) have gastrointestinal (GI) dysfunction, with frequent symptoms including gastroesophageal reflux and constipation. The duplicated region consists of genes encoding for GABA receptor A subunits and GABA is an important neurotransmitter in the Enteric Nervous System (ENS). The gut produces over 90% of the body's serotonin, and serotonin plays a vital role in the enteric neuronal circuitry that regulates gut motility. We investigated GI dysfunction and serotonin-mediated neurotransmission in the ENS. Both male and female adult 15q dup mice had delayed GI transit. We investigated colonic motility using a video imaging approach in which colonic contractions were assessed ex vivo using a video camera and in-house software. When 15q dup mice were treated with Bicuculine, colonic contractions were slower and traveled for a shorter distance. Since the 15q dup neurons were under a hypo-serotonin condition, the potential of Prucalopride to restore the delayed GI transit was investigated. Prucalopride reversed the delayed GI transit in 15q dup mice. The results suggest that enteric neurons in 15q dup mice are more susceptible to GABA receptor inhibition and targeting serotonin receptors is an effective way to treat GI dysfunction in 15q dup syndrome.
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| 現在までの達成度 (段落) |
令和4年度が最終年度であるため、記入しない。
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| 今後の研究の推進方策 |
令和4年度が最終年度であるため、記入しない。
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