Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure

Detalhes bibliográficos
Autor(a) principal: Borges, Sónia Maria de Sousa
Data de Publicação: 2013
Outros Autores: Coimbra, Bárbara Guimarães Salazar, Cunha, Carina Isabel Soares da, Pêgo, José M., Sousa, Nuno, Rodrigues, Ana João
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/1822/25150
Resumo: Prenatal stress or exposure to elevated levels of glucocorticoids (GCs) can impair specific neurobehavioral circuits leading to alterations in emotional processes later in life. In turn, emotional deficits may interfere with the quality and degree of social interaction. Here, by using a comprehensive behavioral approach in combination with the measurement of ultrasonic vocalizations, we show that in utero GC (iuGC)-exposed animals present increased immobility in the forced swimming test, pronounced anhedonic behavior (both anticipatory and consummatory), and an impairment in social interaction at different life stages. Importantly, we also found that social behavioral expression is highly dependent on the affective status of the partner. A profound reduction in mesolimbic dopaminergic transmission was found in iuGC animals, suggesting a key role for dopamine (DA) in the etiology of the observed behavioral deficits. Confirming this idea, we present evidence that a simple pharmacological approach—acute L-3,4-dihydroxyphenylacetic acid (L-DOPA) oral administration, is able to normalize DA levels in iuGC animals, with a concomitant amelioration of several dimensions of the emotional and social behaviors. Interestingly, L-DOPA effects in control individuals were not so straightforward; suggesting that both hypo- and hyperdopaminergia are detrimental in the context of such complex behaviors.
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spelling Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposureAnhedoniaSocial behaviorDopamineMesolimbic circuitDepressionScience & TechnologyPrenatal stress or exposure to elevated levels of glucocorticoids (GCs) can impair specific neurobehavioral circuits leading to alterations in emotional processes later in life. In turn, emotional deficits may interfere with the quality and degree of social interaction. Here, by using a comprehensive behavioral approach in combination with the measurement of ultrasonic vocalizations, we show that in utero GC (iuGC)-exposed animals present increased immobility in the forced swimming test, pronounced anhedonic behavior (both anticipatory and consummatory), and an impairment in social interaction at different life stages. Importantly, we also found that social behavioral expression is highly dependent on the affective status of the partner. A profound reduction in mesolimbic dopaminergic transmission was found in iuGC animals, suggesting a key role for dopamine (DA) in the etiology of the observed behavioral deficits. Confirming this idea, we present evidence that a simple pharmacological approach—acute L-3,4-dihydroxyphenylacetic acid (L-DOPA) oral administration, is able to normalize DA levels in iuGC animals, with a concomitant amelioration of several dimensions of the emotional and social behaviors. Interestingly, L-DOPA effects in control individuals were not so straightforward; suggesting that both hypo- and hyperdopaminergia are detrimental in the context of such complex behaviors.This work was supported by a grant of Institute for the Study of Affective Neuroscience (ISAN) and Janssen Neurosciences Prize. SB and AJR have Fundacao para a Ciencia e Tecnologia (FCT) fellowships (SFRH/BD/89936/2012; SFRH/BPD/33611/2009).Springer NatureUniversidade do MinhoBorges, Sónia Maria de SousaCoimbra, Bárbara Guimarães SalazarCunha, Carina Isabel Soares daPêgo, José M.Sousa, NunoRodrigues, Ana João2013-09-262013-09-26T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/1822/25150eng0893-133X10.1038/npp.2013.10823648781http://www.nature.com/info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-07-21T12:34:07Zoai:repositorium.sdum.uminho.pt:1822/25150Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T19:29:44.444645Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
title Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
spellingShingle Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
Borges, Sónia Maria de Sousa
Anhedonia
Social behavior
Dopamine
Mesolimbic circuit
Depression
Science & Technology
title_short Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
title_full Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
title_fullStr Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
title_full_unstemmed Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
title_sort Dopaminergic modulation of affective and social deficits induced by prenatal glucocorticoid exposure
author Borges, Sónia Maria de Sousa
author_facet Borges, Sónia Maria de Sousa
Coimbra, Bárbara Guimarães Salazar
Cunha, Carina Isabel Soares da
Pêgo, José M.
Sousa, Nuno
Rodrigues, Ana João
author_role author
author2 Coimbra, Bárbara Guimarães Salazar
Cunha, Carina Isabel Soares da
Pêgo, José M.
Sousa, Nuno
Rodrigues, Ana João
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade do Minho
dc.contributor.author.fl_str_mv Borges, Sónia Maria de Sousa
Coimbra, Bárbara Guimarães Salazar
Cunha, Carina Isabel Soares da
Pêgo, José M.
Sousa, Nuno
Rodrigues, Ana João
dc.subject.por.fl_str_mv Anhedonia
Social behavior
Dopamine
Mesolimbic circuit
Depression
Science & Technology
topic Anhedonia
Social behavior
Dopamine
Mesolimbic circuit
Depression
Science & Technology
description Prenatal stress or exposure to elevated levels of glucocorticoids (GCs) can impair specific neurobehavioral circuits leading to alterations in emotional processes later in life. In turn, emotional deficits may interfere with the quality and degree of social interaction. Here, by using a comprehensive behavioral approach in combination with the measurement of ultrasonic vocalizations, we show that in utero GC (iuGC)-exposed animals present increased immobility in the forced swimming test, pronounced anhedonic behavior (both anticipatory and consummatory), and an impairment in social interaction at different life stages. Importantly, we also found that social behavioral expression is highly dependent on the affective status of the partner. A profound reduction in mesolimbic dopaminergic transmission was found in iuGC animals, suggesting a key role for dopamine (DA) in the etiology of the observed behavioral deficits. Confirming this idea, we present evidence that a simple pharmacological approach—acute L-3,4-dihydroxyphenylacetic acid (L-DOPA) oral administration, is able to normalize DA levels in iuGC animals, with a concomitant amelioration of several dimensions of the emotional and social behaviors. Interestingly, L-DOPA effects in control individuals were not so straightforward; suggesting that both hypo- and hyperdopaminergia are detrimental in the context of such complex behaviors.
publishDate 2013
dc.date.none.fl_str_mv 2013-09-26
2013-09-26T00:00:00Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/1822/25150
url http://hdl.handle.net/1822/25150
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 0893-133X
10.1038/npp.2013.108
23648781
http://www.nature.com/
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dc.publisher.none.fl_str_mv Springer Nature
publisher.none.fl_str_mv Springer Nature
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