Utilize este identificador para referenciar este registo:
https://hdl.handle.net/1822/64299
Título: | Lithium prevents stress-induced reduction of vascular endothelium growth factor levels |
Autor(es): | Silva, Rui Martins, Luís Longatto, Adhemar Almeida, Osborne F. X. Sousa, Nuno |
Palavras-chave: | Animals Antimanic Agents Disease Models, Animal Gene Expression Regulation Glycogen Synthase Kinase 3 Glycogen Synthase Kinase 3 beta Hippocampus Lithium Male Nerve Tissue Proteins Rats Rats, Wistar Stress, Physiological Vascular Endothelial Growth Factors beta Catenin Angiogenesis Neurogenesis Chronic mild stress Neuroplasticity |
Data: | 11-Dez-2007 |
Editora: | Elsevier 1 |
Revista: | Neuroscience Letters |
Resumo(s): | Understanding the mechanisms that regulate postnatal neurogenesis is becoming increasingly relevant since its modulation has been implicated in the pathogenesis of certain neuropsychiatric disorders. Lithium is a mood stabilizer known to increase hippocampal neurogenesis. Lithium also results in increased levels of the angiogenic factor vascular endothelial growth factor (VEGF). Since VEGF was recently shown to have neurogenic properties, we were interested to examine whether lithium administration might also be accompanied by alterations in VEGF expression in the hippocampus of normal and stressed rats; the latter treatment was introduced to reproduce some of the psychopathological signs for which lithium is used therapeutically. The expression of VEGF in the hippocampus in stressed animals was lower than that in controls, but the effect of stress was significantly attenuated in animals concomitantly receiving lithium. Double staining for VEGF and specific markers for immature neurons, mature neurons and astroglia revealed that immature neurons were most sensitive to the VEGF-inhibiting effects of stress. Confirming the involvement of a known regulatory pathway in these actions of lithium, we demonstrated that lithium co-administration prevented the stress-induced upregulation of glycogen synthase kinase-3beta (GSK-3beta) and down-regulation of beta-catenin expression; GSK-3beta is a known primary lithium target and its inhibition by this mood stabilizer leads to an upregulation of beta-catenin and subsequently, an increase of VEGF. Our results suggest that the actions of lithium, and possibly its therapeutic efficacy as a mood stabilizer also, are mediated by VEGF. |
Tipo: | Artigo |
URI: | https://hdl.handle.net/1822/64299 |
DOI: | 10.1016/j.neulet.2007.09.062 |
ISSN: | 0304-3940 |
e-ISSN: | 1872-7972 |
Versão da editora: | https://www.sciencedirect.com/science/article/pii/S030439400701052X |
Arbitragem científica: | yes |
Acesso: | Acesso restrito UMinho |
Aparece nas coleções: | ICVS - Artigos em revistas internacionais / Papers in international journals |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
---|---|---|---|---|
Silva-2007-Lithium-prevents-stress-induced-red.pdf Acesso restrito! | 790,37 kB | Adobe PDF | Ver/Abrir |