Prenatal zinc prevents communication impairments and BDNF disturbance in a rat model of autism induced by prenatal lipopolysaccharide exposure
Autor(a) principal: | |
---|---|
Data de Publicação: | 2015 |
Outros Autores: | , , |
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. |
id |
UNSP_7fa9f9f849bcb9741b1c3ec15e4a7127 |
---|---|
oai_identifier_str |
oai:repositorio.unesp.br:11449/158418 |
network_acronym_str |
UNSP |
network_name_str |
Repositório Institucional da UNESP |
repository_id_str |
2946 |
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) |
repository.mail.fl_str_mv |
|
_version_ |
1808128457211641856 |