Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania

Detalhes bibliográficos
Autor(a) principal: Stertz,Laura
Data de Publicação: 2014
Outros Autores: Fries,Gabriel Rodrigo, Aguiar,Bianca Wollenhaupt de, Pfaffenseller,Bianca, Valvassori,Samira S., Gubert,Carolina, Ferreira,Camila L., Moretti,Morgana, Ceresér,Keila M., Kauer-Sant'Anna,Márcia, Quevedo,João, Kapczinski,Flavio
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Psychiatry (São Paulo. 1999. Online)
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462014000100008
Resumo: Objective: In the present study, we aimed to examine the effects of repeated D-amphetamine (AMPH) exposure, a well-accepted animal model of acute mania in bipolar disorder (BD), and histone deacetylase (HDAC) inhibitors on locomotor behavior and HDAC activity in the prefrontal cortex (PFC) and peripheral blood mononuclear cells (PBMCs) of rats. Moreover, we aimed to assess brain-derived neurotrophic factor (BDNF) protein and mRNA levels in these samples. Methods: We treated adult male Wistar rats with 2 mg/kg AMPH or saline intraperitoneally for 14 days. Between the 8th and 14th days, rats also received 47.5 mg/kg lithium (Li), 200 mg/kg sodium valproate (VPT), 2 mg/kg sodium butyrate (SB), or saline. We evaluated locomotor activity in the open-field task and assessed HDAC activity in the PFC and PBMCs, and BDNF levels in the PFC and plasma. Results: AMPH significantly increased locomotor activity, which was reversed by all drugs. This hyperactivity was associated with increased HDAC activity in the PFC, which was partially reversed by Li, VPT, and SB. No differences were found in BDNF levels. Conclusion: Repeated AMPH administration increases HDAC activity in the PFC without altering BDNF levels. The partial reversal of HDAC increase by Li, VPT, and SB may account for their ability to reverse AMPH-induced hyperactivity.
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spelling Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of maniaBipolar disordermood stabilizersodium butyratehistone deacetylaseBDNF Objective: In the present study, we aimed to examine the effects of repeated D-amphetamine (AMPH) exposure, a well-accepted animal model of acute mania in bipolar disorder (BD), and histone deacetylase (HDAC) inhibitors on locomotor behavior and HDAC activity in the prefrontal cortex (PFC) and peripheral blood mononuclear cells (PBMCs) of rats. Moreover, we aimed to assess brain-derived neurotrophic factor (BDNF) protein and mRNA levels in these samples. Methods: We treated adult male Wistar rats with 2 mg/kg AMPH or saline intraperitoneally for 14 days. Between the 8th and 14th days, rats also received 47.5 mg/kg lithium (Li), 200 mg/kg sodium valproate (VPT), 2 mg/kg sodium butyrate (SB), or saline. We evaluated locomotor activity in the open-field task and assessed HDAC activity in the PFC and PBMCs, and BDNF levels in the PFC and plasma. Results: AMPH significantly increased locomotor activity, which was reversed by all drugs. This hyperactivity was associated with increased HDAC activity in the PFC, which was partially reversed by Li, VPT, and SB. No differences were found in BDNF levels. Conclusion: Repeated AMPH administration increases HDAC activity in the PFC without altering BDNF levels. The partial reversal of HDAC increase by Li, VPT, and SB may account for their ability to reverse AMPH-induced hyperactivity. Associação Brasileira de Psiquiatria2014-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462014000100008Brazilian Journal of Psychiatry v.36 n.1 2014reponame:Brazilian Journal of Psychiatry (São Paulo. 1999. Online)instname:Associação Brasileira de Psiquiatria (ABP)instacron:ABP10.1590/1516-4446-2013-1094info:eu-repo/semantics/openAccessStertz,LauraFries,Gabriel RodrigoAguiar,Bianca Wollenhaupt dePfaffenseller,BiancaValvassori,Samira S.Gubert,CarolinaFerreira,Camila L.Moretti,MorganaCeresér,Keila M.Kauer-Sant'Anna,MárciaQuevedo,JoãoKapczinski,Flavioeng2015-04-14T00:00:00Zoai:scielo:S1516-44462014000100008Revistahttp://www.bjp.org.br/ahead_of_print.asphttps://old.scielo.br/oai/scielo-oai.php||rbp@abpbrasil.org.br1809-452X1516-4446opendoar:2015-04-14T00:00Brazilian Journal of Psychiatry (São Paulo. 1999. Online) - Associação Brasileira de Psiquiatria (ABP)false
dc.title.none.fl_str_mv Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
title Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
spellingShingle Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
Stertz,Laura
Bipolar disorder
mood stabilizer
sodium butyrate
histone deacetylase
BDNF
title_short Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
title_full Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
title_fullStr Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
title_full_unstemmed Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
title_sort Histone deacetylase activity and brain-derived neurotrophic factor (BDNF) levels in a pharmacological model of mania
author Stertz,Laura
author_facet Stertz,Laura
Fries,Gabriel Rodrigo
Aguiar,Bianca Wollenhaupt de
Pfaffenseller,Bianca
Valvassori,Samira S.
Gubert,Carolina
Ferreira,Camila L.
Moretti,Morgana
Ceresér,Keila M.
Kauer-Sant'Anna,Márcia
Quevedo,João
Kapczinski,Flavio
author_role author
author2 Fries,Gabriel Rodrigo
Aguiar,Bianca Wollenhaupt de
Pfaffenseller,Bianca
Valvassori,Samira S.
Gubert,Carolina
Ferreira,Camila L.
Moretti,Morgana
Ceresér,Keila M.
Kauer-Sant'Anna,Márcia
Quevedo,João
Kapczinski,Flavio
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Stertz,Laura
Fries,Gabriel Rodrigo
Aguiar,Bianca Wollenhaupt de
Pfaffenseller,Bianca
Valvassori,Samira S.
Gubert,Carolina
Ferreira,Camila L.
Moretti,Morgana
Ceresér,Keila M.
Kauer-Sant'Anna,Márcia
Quevedo,João
Kapczinski,Flavio
dc.subject.por.fl_str_mv Bipolar disorder
mood stabilizer
sodium butyrate
histone deacetylase
BDNF
topic Bipolar disorder
mood stabilizer
sodium butyrate
histone deacetylase
BDNF
description Objective: In the present study, we aimed to examine the effects of repeated D-amphetamine (AMPH) exposure, a well-accepted animal model of acute mania in bipolar disorder (BD), and histone deacetylase (HDAC) inhibitors on locomotor behavior and HDAC activity in the prefrontal cortex (PFC) and peripheral blood mononuclear cells (PBMCs) of rats. Moreover, we aimed to assess brain-derived neurotrophic factor (BDNF) protein and mRNA levels in these samples. Methods: We treated adult male Wistar rats with 2 mg/kg AMPH or saline intraperitoneally for 14 days. Between the 8th and 14th days, rats also received 47.5 mg/kg lithium (Li), 200 mg/kg sodium valproate (VPT), 2 mg/kg sodium butyrate (SB), or saline. We evaluated locomotor activity in the open-field task and assessed HDAC activity in the PFC and PBMCs, and BDNF levels in the PFC and plasma. Results: AMPH significantly increased locomotor activity, which was reversed by all drugs. This hyperactivity was associated with increased HDAC activity in the PFC, which was partially reversed by Li, VPT, and SB. No differences were found in BDNF levels. Conclusion: Repeated AMPH administration increases HDAC activity in the PFC without altering BDNF levels. The partial reversal of HDAC increase by Li, VPT, and SB may account for their ability to reverse AMPH-induced hyperactivity.
publishDate 2014
dc.date.none.fl_str_mv 2014-03-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462014000100008
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462014000100008
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/1516-4446-2013-1094
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Associação Brasileira de Psiquiatria
publisher.none.fl_str_mv Associação Brasileira de Psiquiatria
dc.source.none.fl_str_mv Brazilian Journal of Psychiatry v.36 n.1 2014
reponame:Brazilian Journal of Psychiatry (São Paulo. 1999. Online)
instname:Associação Brasileira de Psiquiatria (ABP)
instacron:ABP
instname_str Associação Brasileira de Psiquiatria (ABP)
instacron_str ABP
institution ABP
reponame_str Brazilian Journal of Psychiatry (São Paulo. 1999. Online)
collection Brazilian Journal of Psychiatry (São Paulo. 1999. Online)
repository.name.fl_str_mv Brazilian Journal of Psychiatry (São Paulo. 1999. Online) - Associação Brasileira de Psiquiatria (ABP)
repository.mail.fl_str_mv ||rbp@abpbrasil.org.br
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