Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/8397

TitleNeuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat
Author(s)Gonçalves, Leonor
Silva, Rui Jorge
Ribeiro, Filipa Pinto
Pêgo, José M.
Bessa, J. M.
Pertovaara, Antti
Sousa, Nuno
Almeida, Armando
KeywordsNeuropathic pain
Amygdala
Adult neurogenesis
Depressive-like behaviour
Issue dateSep-2008
PublisherElsevier
JournalExperimental Neurology
Citation"Experimental Neurology". ISSN 0014-4886. 213 :1 (Sept. 2008) 48-56
Abstract(s)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.
TypeArticle
URIhttp://hdl.handle.net/1822/8397
DOI10.1016/j.expneurol.2008.04.043
ISSN0014-4886
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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