Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.

(±)3,4-Methylenedioxymethamphetamine (MDMA) is a relatively selective dopaminergic neurotoxin in mice. This study was designed to evaluate whether MDMA exposure affects their recognition memory and hippocampal expression of plasticity markers. Mice were administered with increasing doses of MDMA onc...

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Autores: Abad, Sonia, Camarasa García, Jordi, Pubill Sánchez, David, Camins Espuny, Antoni, Escubedo Rafa, Elena
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2015
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/98696
Acceso en línea:https://hdl.handle.net/2445/98696
Access Level:acceso abierto
Palabra clave:Èxtasi (Droga)
Amfetamines
Hipocamp (Cervell)
Trastorns de la memòria
Ratolins (Animals de laboratori)
Ecstasy (Drug)
Amphetamines
Hippocampus (Brain)
Memory disorders
Mice (Laboratory animals)
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oai_identifier_str oai:recercat.cat:2445/98696
network_acronym_str ES
network_name_str España
repository_id_str
spelling Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.Abad, SoniaCamarasa García, JordiPubill Sánchez, DavidCamins Espuny, AntoniEscubedo Rafa, ElenaÈxtasi (Droga)AmfetaminesHipocamp (Cervell)Trastorns de la memòriaRatolins (Animals de laboratori)Ecstasy (Drug)AmphetaminesHippocampus (Brain)Memory disordersMice (Laboratory animals)(±)3,4-Methylenedioxymethamphetamine (MDMA) is a relatively selective dopaminergic neurotoxin in mice. This study was designed to evaluate whether MDMA exposure affects their recognition memory and hippocampal expression of plasticity markers. Mice were administered with increasing doses of MDMA once per week for 8 weeks (three times in 1 day, every 3 h) and killed 2 weeks (2w) or 3 months (3m) later. The treatment did not modify hippocampal tryptophan hydroxylase 2, a serotonergic indicator, but induced an initial reduction in dopaminergic markers in substantia nigra, which remained stable for at least 3 months. In parallel, MDMA produced a decrease in dopamine (DA) levels in the striatum at 2w, which were restored 3 months later, suggesting dopaminergic terminal regeneration (sprouting phenomenon). Moreover, recognition memory was assessed using the object recognition test. Young (2w) and mature (3m) adult mice exhibited impaired memory after 24-h but not after just 1-h retention interval. Two weeks after the treatment, animals showed constant levels of CREB but an increase in its phosphorylated form and in c-Fos expression. Brain-derived neurotrophic factor (BDNF) and especially Arc overexpression was sustained and long-lasting. We cannot rule out the absence of MDMA injury in the hippocampus being due to the generation of BDNF. The levels of NMDAR2B, PSD-95, and synaptophysin were unaffected. In conclusion, the young mice exposed to MDMA showed increased expression of early key markers of plasticity, which sometimes remained for 3 months, and suggests hippocampal maladaptive plasticity that could explain memory deficits evidenced here.Humana Press2016201620152016info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersion13 p.application/pdfhttps://hdl.handle.net/2445/98696Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésVersió postprint del document publicat a: http://dx.doi.org/10.1007/s12035-015-9618-zMolecular Neurobiology, 2015http://dx.doi.org/10.1007/s12035-015-9618-z(c) Humana Press., 2015info:eu-repo/semantics/openAccessoai:recercat.cat:2445/986962026-05-29T05:05:01Z
dc.title.none.fl_str_mv Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
title Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
spellingShingle Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
Abad, Sonia
Èxtasi (Droga)
Amfetamines
Hipocamp (Cervell)
Trastorns de la memòria
Ratolins (Animals de laboratori)
Ecstasy (Drug)
Amphetamines
Hippocampus (Brain)
Memory disorders
Mice (Laboratory animals)
title_short Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
title_full Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
title_fullStr Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
title_full_unstemmed Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
title_sort Adaptive plasticity in the hippocampus of young mice intermittently exposed to MDMA could be the origin of memory deficits.
dc.creator.none.fl_str_mv Abad, Sonia
Camarasa García, Jordi
Pubill Sánchez, David
Camins Espuny, Antoni
Escubedo Rafa, Elena
author Abad, Sonia
author_facet Abad, Sonia
Camarasa García, Jordi
Pubill Sánchez, David
Camins Espuny, Antoni
Escubedo Rafa, Elena
author_role author
author2 Camarasa García, Jordi
Pubill Sánchez, David
Camins Espuny, Antoni
Escubedo Rafa, Elena
author2_role author
author
author
author
dc.subject.none.fl_str_mv Èxtasi (Droga)
Amfetamines
Hipocamp (Cervell)
Trastorns de la memòria
Ratolins (Animals de laboratori)
Ecstasy (Drug)
Amphetamines
Hippocampus (Brain)
Memory disorders
Mice (Laboratory animals)
topic Èxtasi (Droga)
Amfetamines
Hipocamp (Cervell)
Trastorns de la memòria
Ratolins (Animals de laboratori)
Ecstasy (Drug)
Amphetamines
Hippocampus (Brain)
Memory disorders
Mice (Laboratory animals)
description (±)3,4-Methylenedioxymethamphetamine (MDMA) is a relatively selective dopaminergic neurotoxin in mice. This study was designed to evaluate whether MDMA exposure affects their recognition memory and hippocampal expression of plasticity markers. Mice were administered with increasing doses of MDMA once per week for 8 weeks (three times in 1 day, every 3 h) and killed 2 weeks (2w) or 3 months (3m) later. The treatment did not modify hippocampal tryptophan hydroxylase 2, a serotonergic indicator, but induced an initial reduction in dopaminergic markers in substantia nigra, which remained stable for at least 3 months. In parallel, MDMA produced a decrease in dopamine (DA) levels in the striatum at 2w, which were restored 3 months later, suggesting dopaminergic terminal regeneration (sprouting phenomenon). Moreover, recognition memory was assessed using the object recognition test. Young (2w) and mature (3m) adult mice exhibited impaired memory after 24-h but not after just 1-h retention interval. Two weeks after the treatment, animals showed constant levels of CREB but an increase in its phosphorylated form and in c-Fos expression. Brain-derived neurotrophic factor (BDNF) and especially Arc overexpression was sustained and long-lasting. We cannot rule out the absence of MDMA injury in the hippocampus being due to the generation of BDNF. The levels of NMDAR2B, PSD-95, and synaptophysin were unaffected. In conclusion, the young mice exposed to MDMA showed increased expression of early key markers of plasticity, which sometimes remained for 3 months, and suggests hippocampal maladaptive plasticity that could explain memory deficits evidenced here.
publishDate 2015
dc.date.none.fl_str_mv 2015
2016
2016
2016
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/98696
url https://hdl.handle.net/2445/98696
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: http://dx.doi.org/10.1007/s12035-015-9618-z
Molecular Neurobiology, 2015
http://dx.doi.org/10.1007/s12035-015-9618-z
dc.rights.none.fl_str_mv (c) Humana Press., 2015
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) Humana Press., 2015
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 13 p.
application/pdf
dc.publisher.none.fl_str_mv Humana Press
publisher.none.fl_str_mv Humana Press
dc.source.none.fl_str_mv Articles publicats en revistes (Farmacologia, Toxicologia i Química Terapèutica)
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,812429

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