Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure

Detalhes bibliográficos
Autor(a) principal: Kirsten, Thiago B. [UNESP]
Data de Publicação: 2015
Outros Autores: Queiroz-Hazarbassanov, Nicolle, Bernardi, Maria M. [UNESP], Felicio, Luciano F.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.lfs.2015.02.027
http://hdl.handle.net/11449/158418
Resumo: Aims: Previous investigations by our group have shown that prenatal exposure to lipopolysaccharide (LPS), which mimics infections by Gram-negative bacteria, induced autistic-like behavior. No effective treatment yet exists for autism. Therefore, we used our rat model to test a possible treatment for autism. We selected zinc as the prenatal treatment to prevent or ease the impairments induced by LPS because LPS induces hypozincaemia. Materials and methods: We evaluated the effects of LPS and zinc on female reproductive performance. Communication, which is impaired in autism, was tested in pups by ultrasonic vocalizations. Plasma levels of brain-derived neurotrophic factor (BDNF) were determined because it has been considered an autism important biomarker. Key findings: Prenatal LPS exposure reduced offspring number and treatment with zinc prevented this reduction. Moreover, pups that were prenatally exposed to LPS spent longer periods without calling their mothers, and posttreatment with zinc prevented this impairment induced by LPS to the same levels as controls. Prenatal LPS also increased BDNF levels in adult offspring, and posttreatment with zinc reduced the elevation of BDNF to the same levels as controls. Significance: BDNF hyperactivity was also found in several studies of autistic patients. Together with our previous studies, our model of prenatal LPS induced autistic-like behavioral, brain, and immune disturbances. This suggests that it is a valid rat model of autism. Prenatal zinc prevented reproductive, communication, and BDNF impairments. The present study revealed a potential beneficial effect of prenatal zinc administration for the prevention of autism with regard to the BDNF pathway. (c) 2015 Elsevier Inc. All rights reserved.
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spelling Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposureAutistic-like effectsMaternal immune activationPrenatal infectionUltrasonic vocalizationsGestationAims: Previous investigations by our group have shown that prenatal exposure to lipopolysaccharide (LPS), which mimics infections by Gram-negative bacteria, induced autistic-like behavior. No effective treatment yet exists for autism. Therefore, we used our rat model to test a possible treatment for autism. We selected zinc as the prenatal treatment to prevent or ease the impairments induced by LPS because LPS induces hypozincaemia. Materials and methods: We evaluated the effects of LPS and zinc on female reproductive performance. Communication, which is impaired in autism, was tested in pups by ultrasonic vocalizations. Plasma levels of brain-derived neurotrophic factor (BDNF) were determined because it has been considered an autism important biomarker. Key findings: Prenatal LPS exposure reduced offspring number and treatment with zinc prevented this reduction. Moreover, pups that were prenatally exposed to LPS spent longer periods without calling their mothers, and posttreatment with zinc prevented this impairment induced by LPS to the same levels as controls. Prenatal LPS also increased BDNF levels in adult offspring, and posttreatment with zinc reduced the elevation of BDNF to the same levels as controls. Significance: BDNF hyperactivity was also found in several studies of autistic patients. Together with our previous studies, our model of prenatal LPS induced autistic-like behavioral, brain, and immune disturbances. This suggests that it is a valid rat model of autism. Prenatal zinc prevented reproductive, communication, and BDNF impairments. The present study revealed a potential beneficial effect of prenatal zinc administration for the prevention of autism with regard to the BDNF pathway. (c) 2015 Elsevier Inc. All rights reserved.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ Sao Paulo, Dept Pathol, Sch Vet Med, BR-05508270 Sao Paulo, SP, BrazilUniv Estadual Paulista, Environm & Expt Pathol, BR-04026002 Sao Paulo, SP, BrazilUniv Estadual Paulista, Environm & Expt Pathol, BR-04026002 Sao Paulo, SP, BrazilFAPESP: 2012/07007-8FAPESP: 2009/51886-3CAPES: CAPES/Premio 1029/2014Elsevier B.V.Universidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Kirsten, Thiago B. [UNESP]Queiroz-Hazarbassanov, NicolleBernardi, Maria M. [UNESP]Felicio, Luciano F.2018-11-26T15:27:35Z2018-11-26T15:27:35Z2015-06-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article12-17application/pdfhttp://dx.doi.org/10.1016/j.lfs.2015.02.027Life Sciences. Oxford: Pergamon-elsevier Science Ltd, v. 130, p. 12-17, 2015.0024-3205http://hdl.handle.net/11449/15841810.1016/j.lfs.2015.02.027WOS:000354756200003WOS:000354756200003.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengLife Sciences1,071info:eu-repo/semantics/openAccess2023-10-16T06:04:46Zoai:repositorio.unesp.br:11449/158418Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T15:05:14.324298Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
title Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
spellingShingle Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
Kirsten, Thiago B. [UNESP]
Autistic-like effects
Maternal immune activation
Prenatal infection
Ultrasonic vocalizations
Gestation
title_short Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
title_full Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
title_fullStr Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
title_full_unstemmed Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
title_sort Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
author Kirsten, Thiago B. [UNESP]
author_facet Kirsten, Thiago B. [UNESP]
Queiroz-Hazarbassanov, Nicolle
Bernardi, Maria M. [UNESP]
Felicio, Luciano F.
author_role author
author2 Queiroz-Hazarbassanov, Nicolle
Bernardi, Maria M. [UNESP]
Felicio, Luciano F.
author2_role author
author
author
dc.contributor.none.fl_str_mv Universidade de São Paulo (USP)
Universidade Estadual Paulista (Unesp)
dc.contributor.author.fl_str_mv Kirsten, Thiago B. [UNESP]
Queiroz-Hazarbassanov, Nicolle
Bernardi, Maria M. [UNESP]
Felicio, Luciano F.
dc.subject.por.fl_str_mv Autistic-like effects
Maternal immune activation
Prenatal infection
Ultrasonic vocalizations
Gestation
topic Autistic-like effects
Maternal immune activation
Prenatal infection
Ultrasonic vocalizations
Gestation
description Aims: Previous investigations by our group have shown that prenatal exposure to lipopolysaccharide (LPS), which mimics infections by Gram-negative bacteria, induced autistic-like behavior. No effective treatment yet exists for autism. Therefore, we used our rat model to test a possible treatment for autism. We selected zinc as the prenatal treatment to prevent or ease the impairments induced by LPS because LPS induces hypozincaemia. Materials and methods: We evaluated the effects of LPS and zinc on female reproductive performance. Communication, which is impaired in autism, was tested in pups by ultrasonic vocalizations. Plasma levels of brain-derived neurotrophic factor (BDNF) were determined because it has been considered an autism important biomarker. Key findings: Prenatal LPS exposure reduced offspring number and treatment with zinc prevented this reduction. Moreover, pups that were prenatally exposed to LPS spent longer periods without calling their mothers, and posttreatment with zinc prevented this impairment induced by LPS to the same levels as controls. Prenatal LPS also increased BDNF levels in adult offspring, and posttreatment with zinc reduced the elevation of BDNF to the same levels as controls. Significance: BDNF hyperactivity was also found in several studies of autistic patients. Together with our previous studies, our model of prenatal LPS induced autistic-like behavioral, brain, and immune disturbances. This suggests that it is a valid rat model of autism. Prenatal zinc prevented reproductive, communication, and BDNF impairments. The present study revealed a potential beneficial effect of prenatal zinc administration for the prevention of autism with regard to the BDNF pathway. (c) 2015 Elsevier Inc. All rights reserved.
publishDate 2015
dc.date.none.fl_str_mv 2015-06-01
2018-11-26T15:27:35Z
2018-11-26T15:27:35Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.lfs.2015.02.027
Life Sciences. Oxford: Pergamon-elsevier Science Ltd, v. 130, p. 12-17, 2015.
0024-3205
http://hdl.handle.net/11449/158418
10.1016/j.lfs.2015.02.027
WOS:000354756200003
WOS:000354756200003.pdf
url http://dx.doi.org/10.1016/j.lfs.2015.02.027
http://hdl.handle.net/11449/158418
identifier_str_mv Life Sciences. Oxford: Pergamon-elsevier Science Ltd, v. 130, p. 12-17, 2015.
0024-3205
10.1016/j.lfs.2015.02.027
WOS:000354756200003
WOS:000354756200003.pdf
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Life Sciences
1,071
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 12-17
application/pdf
dc.publisher.none.fl_str_mv Elsevier B.V.
publisher.none.fl_str_mv Elsevier B.V.
dc.source.none.fl_str_mv Web of Science
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
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