Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/44809

TitleAbsence of IFN gamma promotes hippocampal plasticity and enhances cognitive performance
Author(s)Monteiro, S.
Ferreira, F. M.
Pinto, V.
Roque, Susana
Morais, M
Calçada, Daniela Alexandra Sá
Mota, C.
Correia-Neves, M.
Cerqueira, João José
Issue date2016
PublisherNature Publishing Group
JournalTranslational Psychiatry
CitationMonteiro, 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
Abstract(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.
TypeArticle
URIhttp://hdl.handle.net/1822/44809
DOI10.1038/tp.2015.194
ISSN2158-3188
Publisher versionhttp://www.nature.com/tp/index.html
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em Revistas Internacionais com Referee

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