L773:1090 2139 OR L773:0889 1591
Sökning: L773:1090 2139 OR L773:0889 1591 > Molecular mechanism...
- 45 av 204
- Föregående post
- Nästa post
- Till träfflistan
Molecular mechanisms involved in interleukin 1-beta (IL-1 beta)-induced memory impairment. Modulation by alpha-melanocyte-stimulating hormone (alpha-MSH)
- Gonzalez, P. (författare)
- Machado, I. (författare)
- Vilcaes, A. (författare)
- visa fler...
- Caruso, C. (författare)
- Roth, G. A. (författare)
- Lasaga, M. (författare)
- Scimonelli, T. (författare)
- visa färre...
- (creator_code:org_t)
- Elsevier BV, 2013
- 2013
- Engelska.
- Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 0889-1591 .- 1090-2139. ; 34, s. 141-150
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- 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.
Nyckelord
- IL-1 beta
- Memory consolidation
- alpha-MSH
- Glutamate release
- p38
- ERK
- BDNF
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
- Brain, behavior, and immunity (Sök värdpublikationen i LIBRIS)
Till lärosätets databas
- 45 av 204
- Föregående post
- Nästa post
- Till träfflistan
Hitta mer i SwePub
- Av författaren/redakt...
- Gonzalez, P.
- Machado, I.
- Vilcaes, A.
- Caruso, C.
- Roth, G. A.
- Schiöth, Helgi B ...
- visa fler...
- Lasaga, M.
- Scimonelli, T.
- visa färre...
- Artiklar i publikationen
- Brain, behavior, ...
- Av lärosätet
- Uppsala universitet
Sök utanför SwePub
- Sök vidare i:
- Google Book Search
- Google Scholar
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.
- Copyright © LIBRIS - Nationella bibliotekssystem
- LIBRIS.kb.se
