Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 34, Issue -, Pages 141-150Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2013.08.007
Keywords
IL-1 beta; Memory consolidation; alpha-MSH; Glutamate release; p38; ERK; BDNF
Categories
Funding
- Agencia Nacional de Promocion Cientifica y Tecnologica
- University of Buenos Aires
- Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET)
- Universidad Nacional de Cordoba, Argentina
- Swedish Research Council
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Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-1 beta (IL-1 beta) influences the consolidation of hippocampus-dependent memories. We previously reported that administration of IL-1 beta in dorsal hippocampus impaired contextual fear memory consolidation. Different mechanisms have been implicated in the action of IL-1 beta on long-term potentiation (LTP), but the processes by which this inhibition occurs in vivo remain to be elucidated. We herein report that intrahippocampal injection of IL-1 beta induced a significant increase in p38 phosphorylation after contextual fear conditioning. Also, treatment with SB203580, an inhibitor of p38, reversed impairment induced by IL-1 beta on conditioned fear behavior, indicating that this MAPK would be involved in the effect of the cytokine. We also showed that IL-1 beta administration produced a decrease in glutamate release from dorsal hippocampus synaptosomes and that treatment with SB203580 partially reversed this effect. Our results indicated that IL-1 beta-induced impairment in memory consolidation could be mediated by a decrease in glutamate release. This hypothesis is sustained by the fact that treatment with D-cycloserine (DCS), a partial agonist of the NMDA receptor, reversed the effect of IL-1 beta on contextual fear memory. Furthermore, we demonstrated that IL-1 beta produced a temporal delay in ERK phosphorylation and that DCS administration reversed this effect. We also observed that intrahippocampal injection of IL-1 beta decreased BDNF expression after contextual fear conditioning. We previously demonstrated that alpha-MSH reversed the detrimental effect of IL-1 beta on memory consolidation. The present results demonstrate that alpha-MSH administration did not modify the decrease in glutamate release induced by IL-1 beta. However, intrahippocampal injection of alpha-MSH prevented the effect on ERR phosphorylation and BDNF expression induced by IL-1 beta after contextual fear conditioning. Therefore, in the present study we determine possible molecular mechanisms involved in the impairment induced by IL-1 beta on fear memory consolidation. We also established how this effect could be modulated by alpha-MSH. (C) 2013 Elsevier Inc. All rights reserved.
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