Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , , , |
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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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 instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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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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