Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors

Chiharu Hidaka,1,2 Taiki Kashio,1 Daiju Uchigaki,3 Shinichi Mitsui1,3 1Department of Rehabilitation Sciences, Gunma University Graduate School of Health Sciences, Maebashi, Japan; 2Department of Neurobiology and Anatomy, Kochi Medical School, Kochi University, Nankoku, Japan; 3Department of Occupat...

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Autores principales:	Hidaka C, Kashio T, Uchigaki D, Mitsui S
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2018
Materias:	Early-life stress Mental retardation Neurotrypsin PFC PRSS12 Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/262cb5e4ece64fa5a4a41920a9ba3af0
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spelling	oai:doaj.org-article:262cb5e4ece64fa5a4a41920a9ba3af02021-12-02T04:50:35ZVulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors1178-2021https://doaj.org/article/262cb5e4ece64fa5a4a41920a9ba3af02018-09-01T00:00:00Zhttps://www.dovepress.com/vulnerability-or-resilience-of-motopsin-knockout-mice-to-maternal-sepa-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021Chiharu Hidaka,1,2 Taiki Kashio,1 Daiju Uchigaki,3 Shinichi Mitsui1,3 1Department of Rehabilitation Sciences, Gunma University Graduate School of Health Sciences, Maebashi, Japan; 2Department of Neurobiology and Anatomy, Kochi Medical School, Kochi University, Nankoku, Japan; 3Department of Occupational Therapy, Gunma University, Maebashi, Japan Background: Both environmental and genetic conditions contribute to the robust development of neuronal circuits and adulthood behaviors. Loss of motopsin gene function causes severe intellectual disability in humans and enhanced social behavior in mice. Furthermore, childhood maltreatment is a risk factor for some psychiatric disorders, and children with disabilities have a higher risk of abuse than healthy children. Materials and methods: In this study, we investigated the effects of maternal separation (MS) on adulthood behaviors of motopsin knockout (KO) and wild-type (WT) mice. Results: The MS paradigm decreased the duration that WT mice stayed in the center area of an open field, but not for motopsin KO mice; however, it decreased the novel object recognition index in both genotypes. In the marble burying test, motopsin KO mice buried fewer marbles than WT mice, regardless of the rearing conditions. The MS paradigm slightly increased and reduced open arm entry in the elevated plus maze by WT and motopsin KO mice, respectively. In the three-chamber test, the rate of sniffing the animal cage was increased by the MS paradigm only for motopsin KO mice. After the three-chamber test, motopsin KO mice had fewer cFos-positive cells in the prelimbic cortex, which is involved in emotional response, than WT mice. In the infralimbic cortex, the MS paradigm decreased the number of cFos-positive cells in motopsin KO mice. Conclusion: Our results suggest that motopsin deficiency and childhood adversity independently affect some behaviors, but they may interfere with each other for other behaviors. Defective neuronal circuits in the prefrontal cortex may add to this complexity. Keywords: early-life stress, mental retardation, neurotrypsin, PFC, PRSS12Hidaka CKashio TUchigaki DMitsui SDove Medical PressarticleEarly-life stressMental retardationNeurotrypsinPFCPRSS12Neurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol Volume 14, Pp 2255-2268 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Early-life stress Mental retardation Neurotrypsin PFC PRSS12 Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
spellingShingle	Early-life stress Mental retardation Neurotrypsin PFC PRSS12 Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Hidaka C Kashio T Uchigaki D Mitsui S Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
description	Chiharu Hidaka,1,2 Taiki Kashio,1 Daiju Uchigaki,3 Shinichi Mitsui1,3 1Department of Rehabilitation Sciences, Gunma University Graduate School of Health Sciences, Maebashi, Japan; 2Department of Neurobiology and Anatomy, Kochi Medical School, Kochi University, Nankoku, Japan; 3Department of Occupational Therapy, Gunma University, Maebashi, Japan Background: Both environmental and genetic conditions contribute to the robust development of neuronal circuits and adulthood behaviors. Loss of motopsin gene function causes severe intellectual disability in humans and enhanced social behavior in mice. Furthermore, childhood maltreatment is a risk factor for some psychiatric disorders, and children with disabilities have a higher risk of abuse than healthy children. Materials and methods: In this study, we investigated the effects of maternal separation (MS) on adulthood behaviors of motopsin knockout (KO) and wild-type (WT) mice. Results: The MS paradigm decreased the duration that WT mice stayed in the center area of an open field, but not for motopsin KO mice; however, it decreased the novel object recognition index in both genotypes. In the marble burying test, motopsin KO mice buried fewer marbles than WT mice, regardless of the rearing conditions. The MS paradigm slightly increased and reduced open arm entry in the elevated plus maze by WT and motopsin KO mice, respectively. In the three-chamber test, the rate of sniffing the animal cage was increased by the MS paradigm only for motopsin KO mice. After the three-chamber test, motopsin KO mice had fewer cFos-positive cells in the prelimbic cortex, which is involved in emotional response, than WT mice. In the infralimbic cortex, the MS paradigm decreased the number of cFos-positive cells in motopsin KO mice. Conclusion: Our results suggest that motopsin deficiency and childhood adversity independently affect some behaviors, but they may interfere with each other for other behaviors. Defective neuronal circuits in the prefrontal cortex may add to this complexity. Keywords: early-life stress, mental retardation, neurotrypsin, PFC, PRSS12
format	article
author	Hidaka C Kashio T Uchigaki D Mitsui S
author_facet	Hidaka C Kashio T Uchigaki D Mitsui S
author_sort	Hidaka C
title	Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
title_short	Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
title_full	Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
title_fullStr	Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
title_full_unstemmed	Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
title_sort	vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors
publisher	Dove Medical Press
publishDate	2018
url	https://doaj.org/article/262cb5e4ece64fa5a4a41920a9ba3af0
work_keys_str_mv	AT hidakac vulnerabilityorresilienceofmotopsinknockoutmicetomaternalseparationstressdependingonadulthoodbehaviors AT kashiot vulnerabilityorresilienceofmotopsinknockoutmicetomaternalseparationstressdependingonadulthoodbehaviors AT uchigakid vulnerabilityorresilienceofmotopsinknockoutmicetomaternalseparationstressdependingonadulthoodbehaviors AT mitsuis vulnerabilityorresilienceofmotopsinknockoutmicetomaternalseparationstressdependingonadulthoodbehaviors
_version_	1718400996792598528

Vulnerability or resilience of motopsin knockout mice to maternal separation stress depending on adulthood behaviors

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