Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat

Detalhes bibliográficos
Autor(a) principal: Gonçalves, Leonor
Data de Publicação: 2008
Outros Autores: Silva, Rui Jorge, Ribeiro, Filipa Pinto, Pêgo, José M., Bessa, J. M., Pertovaara, Antti, Sousa, Nuno, Almeida, Armando
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/1822/8397
Resumo: Chronic pain is associated with the development of affective disorders but the underlying mechanisms are not fully understood. Changes in brain centres implicated in both emotional and pain processing are likely to be critical in the interplay of pain control and affective emotional behaviour. In the present study, we assessed emotional behaviour and performed a structural analysis of the amygdala (AMY) in neuropathic rats after two months of hyperalgesia and allodynia, induced by the spared nerve injury model (SNI). When compared with Sham-controls, SNI animals displayed signs of depressive-like behaviour. In addition, we found an increased amygdalar volume in SNI rats. No alterations were found in the dendritic arborizations of AMY neurons but, surprisingly, the amygdalar hypertrophy was associated with an increased cell proliferation [bromodeoxyuridine (BrdU)-positive cells] in the central (CeA) and basolateral (BLA) amygdaloid nuclei. The phenotypic analysis of the newly-acquired cells revealed that they co-label for neuronal markers (BrdU + NeuN and BrdU + Calbindin), but not for differentiated glial cells (BrdU + glial fibrillary acidic protein). We demonstrate that neuropathic pain promotes generation of new neurons in the AMY. Given the established role of the AMY in emotional behaviour, we propose that these neuroplastic changes might contribute for the development of depressive-like symptoms that are usually present in prolonged pain syndromes in humans.
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spelling Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the ratNeuropathic painAmygdalaAdult neurogenesisDepressive-like behaviourScience & TechnologyChronic pain is associated with the development of affective disorders but the underlying mechanisms are not fully understood. Changes in brain centres implicated in both emotional and pain processing are likely to be critical in the interplay of pain control and affective emotional behaviour. In the present study, we assessed emotional behaviour and performed a structural analysis of the amygdala (AMY) in neuropathic rats after two months of hyperalgesia and allodynia, induced by the spared nerve injury model (SNI). When compared with Sham-controls, SNI animals displayed signs of depressive-like behaviour. In addition, we found an increased amygdalar volume in SNI rats. No alterations were found in the dendritic arborizations of AMY neurons but, surprisingly, the amygdalar hypertrophy was associated with an increased cell proliferation [bromodeoxyuridine (BrdU)-positive cells] in the central (CeA) and basolateral (BLA) amygdaloid nuclei. The phenotypic analysis of the newly-acquired cells revealed that they co-label for neuronal markers (BrdU + NeuN and BrdU + Calbindin), but not for differentiated glial cells (BrdU + glial fibrillary acidic protein). We demonstrate that neuropathic pain promotes generation of new neurons in the AMY. Given the established role of the AMY in emotional behaviour, we propose that these neuroplastic changes might contribute for the development of depressive-like symptoms that are usually present in prolonged pain syndromes in humans.Fundação para a Ciência e Tecnologia (FCT) Project no. POCTI/NSE/46399/2002FEDERFundação Calouste Gulbenkian Project no. 74551ElsevierUniversidade do MinhoGonçalves, LeonorSilva, Rui JorgeRibeiro, Filipa PintoPêgo, José M.Bessa, J. M.Pertovaara, AnttiSousa, NunoAlmeida, Armando2008-092008-09-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/1822/8397eng"Experimental Neurology". ISSN 0014-4886. 213 :1 (Sept. 2008) 48-560014-488610.1016/j.expneurol.2008.04.04318599044info: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:RCAAP2023-07-21T12:05:50Zoai:repositorium.sdum.uminho.pt:1822/8397Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T18:56:23.912410Repositório 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 Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
title Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
spellingShingle Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
Gonçalves, Leonor
Neuropathic pain
Amygdala
Adult neurogenesis
Depressive-like behaviour
Science & Technology
title_short Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
title_full Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
title_fullStr Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
title_full_unstemmed Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
title_sort Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
author Gonçalves, Leonor
author_facet Gonçalves, Leonor
Silva, Rui Jorge
Ribeiro, Filipa Pinto
Pêgo, José M.
Bessa, J. M.
Pertovaara, Antti
Sousa, Nuno
Almeida, Armando
author_role author
author2 Silva, Rui Jorge
Ribeiro, Filipa Pinto
Pêgo, José M.
Bessa, J. M.
Pertovaara, Antti
Sousa, Nuno
Almeida, Armando
author2_role author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidade do Minho
dc.contributor.author.fl_str_mv Gonçalves, Leonor
Silva, Rui Jorge
Ribeiro, Filipa Pinto
Pêgo, José M.
Bessa, J. M.
Pertovaara, Antti
Sousa, Nuno
Almeida, Armando
dc.subject.por.fl_str_mv Neuropathic pain
Amygdala
Adult neurogenesis
Depressive-like behaviour
Science & Technology
topic Neuropathic pain
Amygdala
Adult neurogenesis
Depressive-like behaviour
Science & Technology
description Chronic pain is associated with the development of affective disorders but the underlying mechanisms are not fully understood. Changes in brain centres implicated in both emotional and pain processing are likely to be critical in the interplay of pain control and affective emotional behaviour. In the present study, we assessed emotional behaviour and performed a structural analysis of the amygdala (AMY) in neuropathic rats after two months of hyperalgesia and allodynia, induced by the spared nerve injury model (SNI). When compared with Sham-controls, SNI animals displayed signs of depressive-like behaviour. In addition, we found an increased amygdalar volume in SNI rats. No alterations were found in the dendritic arborizations of AMY neurons but, surprisingly, the amygdalar hypertrophy was associated with an increased cell proliferation [bromodeoxyuridine (BrdU)-positive cells] in the central (CeA) and basolateral (BLA) amygdaloid nuclei. The phenotypic analysis of the newly-acquired cells revealed that they co-label for neuronal markers (BrdU + NeuN and BrdU + Calbindin), but not for differentiated glial cells (BrdU + glial fibrillary acidic protein). We demonstrate that neuropathic pain promotes generation of new neurons in the AMY. Given the established role of the AMY in emotional behaviour, we propose that these neuroplastic changes might contribute for the development of depressive-like symptoms that are usually present in prolonged pain syndromes in humans.
publishDate 2008
dc.date.none.fl_str_mv 2008-09
2008-09-01T00:00:00Z
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://hdl.handle.net/1822/8397
url http://hdl.handle.net/1822/8397
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv "Experimental Neurology". ISSN 0014-4886. 213 :1 (Sept. 2008) 48-56
0014-4886
10.1016/j.expneurol.2008.04.043
18599044
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
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instname_str Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
instacron_str RCAAP
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reponame_str Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
collection Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
repository.name.fl_str_mv Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação
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