Impaired interleukin-1beta and c-Fos expression in the hippocampus is associated with a spatial memory deficit in P2X(7) receptor-deficient mice.
PLoS ONE. 2009-06-23; 4(6): e6006
DOI: 10.1371/journal.pone.0006006
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1. PLoS One. 2009 Jun 23;4(6):e6006. doi: 10.1371/journal.pone.0006006.
Impaired interleukin-1beta and c-Fos expression in the hippocampus is associated
with a spatial memory deficit in P2X(7) receptor-deficient mice.
Labrousse VF(1), Costes L, Aubert A, Darnaudéry M, Ferreira G, Amédée T, Layé S.
Author information:
(1)Psychoneuroimmunologie, Nutrition et Génétique (PsyNuGen), INRA UMR 1286, CNRS
UMR 5226, Université de Bordeaux, Bordeaux, France.
Recent evidence suggests that interleukin-1beta (IL-1beta), which was originally
identified as a proinflammatory cytokine, is also required in the brain for
memory processes. We have previously shown that IL-1beta synthesis in the
hippocampus is dependent on P2X(7) receptor (P2X(7)R), which is an ionotropic
receptor of ATP. To substantiate the role of P2X(7)R in both brain IL-1beta
expression and memory processes, we examined the induction of IL-1beta mRNA
expression in the hippocampus of wild-type (WT) and homozygous P2X(7) receptor
knockout mice (P2X(7)R(-/-)) following a spatial memory task. The spatial
recognition task induced both IL-1beta mRNA expression and c-Fos protein
activation in the hippocampus of WT but not of P2X(7)R(-/-) mice. Remarkably,
P2X(7)R(-/-) mice displayed spatial memory impairment in a hippocampal-dependant
task, while their performances in an object recognition task were unaltered.
Taken together, our results show that P2X(7)R plays a critical role in spatial
memory processes and the associated hippocampal IL-1beta mRNA synthesis and c-Fos
activation.
DOI: 10.1371/journal.pone.0006006
PMCID: PMC2695542
PMID: 19547756 [Indexed for MEDLINE]