Utilize este identificador para referenciar este registo: http://hdl.handle.net/1822/44809

TítuloAbsence of IFN gamma promotes hippocampal plasticity and enhances cognitive performance
Autor(es)Monteiro, S.
Ferreira, F. M.
Pinto, V.
Roque, Susana
Morais, M
Calçada, Daniela Alexandra Sá
Mota, C.
Correia-Neves, M.
Cerqueira, João José
Data2016
EditoraNature Publishing Group
RevistaTranslational Psychiatry
CitaçãoMonteiro, S., Ferreira, F. M., Pinto, V., Roque, S., Morais, M., de Sa-Calcada, D., . . . Cerqueira, J. J. (2016). Absence of IFN gamma promotes hippocampal plasticity and enhances cognitive performance. Translational Psychiatry, 6. doi: 10.1038/tp.2015.194
Resumo(s)Cognitive functioning can be differentially modulated by components of the immune system. Interferon-γ (IFNγ) is a pro-inflammatory cytokine whose production is altered in many conditions displaying some degree of cognitive deficits, although its role in cognitive functioning is still unclear. Here we show that the absence of IFNγ selectively enhances cognitive behaviours in tasks in which the hippocampus is implicated. Moreover, the absence of IFNγ leads to volumetric and cell density changes that are restricted to the dorsal part of the hippocampus. In the dorsal hippocampus, the absence of this pro-inflammatory cytokine leads to an increase in the numbers of newly born neurons in the subgranular zone of the dentate gyrus (DG), an adult neurogenic niche known to support learning and memory, and to an enlargement of the dendritic arborization of DG granule and cornu ammonis (CA)1 pyramidal neurons. Moreover, it also modestly impacts synaptic plasticity, by decreasing the paired-pulse facilitation in the Schaffer collateral to CA1 pyramidal cell synapses. Taken together, our results provide evidence that IFNγ is a negative regulator of hippocampal functioning, as its absence positively impacts on dorsal hippocampus structure, cell density, neuronal morphology and synaptic plasticity. Importantly, these neuroplastic changes are associated with improved performance in learning and memory tasks. Therefore, blockage of the IFNγ signalling may present as promising therapeutic targets for the treatment of inflammationassociated cognitive dysfunction.
Tipoarticle
URIhttp://hdl.handle.net/1822/44809
DOI10.1038/tp.2015.194
ISSN2158-3188
Versão da editorahttp://www.nature.com/tp/index.html
Arbitragem científicayes
AcessoopenAccess
Aparece nas coleções:ICVS - Artigos em Revistas Internacionais com Referee

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