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Please use this identifier to cite or link to this item: http://hdl.handle.net/10451/6697

Título: Enhancement of LTP in aged rats is dependent on endogenous BDNF
Autor: Diógenes, Maria J
Costenla, Ana R
Lopes, Luísa V
Jerónimo-Santos, André
Sousa, Vasco C
Fontinha, Bruno M
Ribeiro, Joaquim A
Sebastião, Ana M
Palavras-chave: LTP
Aging
BDNF
Adenosine
A2A receptors
Hippocampus
Issue Date: 2011
Editora: American College of Neuropsychopharmacology
Citação: Neuropsychopharmacology (2011) 36, 1823–1836
Resumo: Long-term potentiation (LTP), considered the neurophysiological basis for learning and memory, is facilitated by brain-derived neurotrophic factor (BDNF), an action more evident when LTP is evoked by weak θ-burst stimuli and dependent on co-activation of adenosine A2A receptors (A2AR), which are more expressed in aged rats. As θ-burst stimuli also favor LTP in aged animals, we hypothesized that enhanced LTP in aging could be related to changes in neuromodulation by BDNF. The magnitude of CA1 LTP induced by a weak θ-burst stimuli delivered to the Schaffer collaterals was significantly higher in hippocampal slices taken from 36 to 38 and from 70 to 80-week-old rats, when compared with LTP magnitude in slices from 4 or 10 to 15-week-old rats; this enhancement does not impact in cognitive improvement as aged rats revealed an impairment on hippocampal-dependent learning and memory performance, as assessed by the Morris water maze tests. The scavenger for BDNF, TrkB-Fc, and the inhibitor of Trk phosphorylation, K252a, attenuated LTP in slices from 70 to 80-week-old rats, but not from 10 to 15-week-old rats. When exogenously added, BDNF significantly increased LTP in slices from 4 and 10 to 15-week-old rats, but did not further increased LTP in 36 to 38 or 70 to 80-week-old rats. The effects of exogenous BDNF on LTP were prevented by the A2AR antagonist, SCH58261 (7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine). These results indicate that the higher LTP magnitude observed upon aging, which does not translate into improved spatial memory performance, is a consequence of an increase in the tonic action of endogenous BDNF.
Descrição: © 2011 American College of Neuropsychopharmacology.
Arbitragem científica: yes
URI: http://dx.doi.org/10.1038/npp.2011.64
http://hdl.handle.net/10451/6697
ISSN: 0893-133X
Versão do Editor: http://www.nature.com/npp/journal/v36/n9/pdf/npp201164a.pdf
Appears in Collections:FM-IFN-Artigos em Revistas Internacionais

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