Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.

Autism spectrum disorders (ASDs) have garnered significant attention as an important grouping of developmental brain disorders. Recent genomic studies have revealed that inherited or de novo copy number variations (CNVs) are significantly involved in the pathophysiology of ASDs. In a previous report...

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Autores principales:	Kota Tamada, Shozo Tomonaga, Fumiyuki Hatanaka, Nobuhiro Nakai, Keizo Takao, Tsuyoshi Miyakawa, Jin Nakatani, Toru Takumi
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/bbe8e3d0432546138e38f9759f8c973b
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spelling	oai:doaj.org-article:bbe8e3d0432546138e38f9759f8c973b2021-11-18T07:01:39ZDecreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.1932-620310.1371/journal.pone.0015126https://doaj.org/article/bbe8e3d0432546138e38f9759f8c973b2010-12-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21179543/?tool=EBIhttps://doaj.org/toc/1932-6203Autism spectrum disorders (ASDs) have garnered significant attention as an important grouping of developmental brain disorders. Recent genomic studies have revealed that inherited or de novo copy number variations (CNVs) are significantly involved in the pathophysiology of ASDs. In a previous report from our laboratory, we generated mice with CNVs as a model of ASDs, with a duplicated mouse chromosome 7C that is orthologous to human chromosome 15q11-13. Behavioral analyses revealed paternally duplicated (patDp/+) mice displayed abnormal behaviors resembling the symptoms of ASDs. In the present study, we extended these findings by performing various behavioral tests with C57BL/6J patDp/+ mice, and comprehensively measuring brain monoamine levels with ex vivo high performance liquid chromatography. Compared with wild-type controls, patDp/+ mice exhibited decreased locomotor and exploratory activities in the open field test, Y-maze test, and fear-conditioning test. Furthermore, their decreased activity levels overcame increased appetite induced by 24 hours of food deprivation in the novelty suppressed feeding test. Serotonin levels in several brain regions of adult patDp/+ mice were lower than those of wild-type control, with no concurrent changes in brain levels of dopamine or norepinephrine. Moreover, analysis of monoamines in postnatal developmental stages demonstrated reduced brain levels of serotonin in young patDp/+ mice. These findings suggest that a disrupted brain serotonergic system, especially during postnatal development, may generate the phenotypes of patDp/+ mice.Kota TamadaShozo TomonagaFumiyuki HatanakaNobuhiro NakaiKeizo TakaoTsuyoshi MiyakawaJin NakataniToru TakumiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 12, p e15126 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kota Tamada Shozo Tomonaga Fumiyuki Hatanaka Nobuhiro Nakai Keizo Takao Tsuyoshi Miyakawa Jin Nakatani Toru Takumi Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
description	Autism spectrum disorders (ASDs) have garnered significant attention as an important grouping of developmental brain disorders. Recent genomic studies have revealed that inherited or de novo copy number variations (CNVs) are significantly involved in the pathophysiology of ASDs. In a previous report from our laboratory, we generated mice with CNVs as a model of ASDs, with a duplicated mouse chromosome 7C that is orthologous to human chromosome 15q11-13. Behavioral analyses revealed paternally duplicated (patDp/+) mice displayed abnormal behaviors resembling the symptoms of ASDs. In the present study, we extended these findings by performing various behavioral tests with C57BL/6J patDp/+ mice, and comprehensively measuring brain monoamine levels with ex vivo high performance liquid chromatography. Compared with wild-type controls, patDp/+ mice exhibited decreased locomotor and exploratory activities in the open field test, Y-maze test, and fear-conditioning test. Furthermore, their decreased activity levels overcame increased appetite induced by 24 hours of food deprivation in the novelty suppressed feeding test. Serotonin levels in several brain regions of adult patDp/+ mice were lower than those of wild-type control, with no concurrent changes in brain levels of dopamine or norepinephrine. Moreover, analysis of monoamines in postnatal developmental stages demonstrated reduced brain levels of serotonin in young patDp/+ mice. These findings suggest that a disrupted brain serotonergic system, especially during postnatal development, may generate the phenotypes of patDp/+ mice.
format	article
author	Kota Tamada Shozo Tomonaga Fumiyuki Hatanaka Nobuhiro Nakai Keizo Takao Tsuyoshi Miyakawa Jin Nakatani Toru Takumi
author_facet	Kota Tamada Shozo Tomonaga Fumiyuki Hatanaka Nobuhiro Nakai Keizo Takao Tsuyoshi Miyakawa Jin Nakatani Toru Takumi
author_sort	Kota Tamada
title	Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
title_short	Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
title_full	Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
title_fullStr	Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
title_full_unstemmed	Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
title_sort	decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/bbe8e3d0432546138e38f9759f8c973b
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Decreased exploratory activity in a mouse model of 15q duplication syndrome; implications for disturbance of serotonin signaling.

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