Molecular mechanisms involved in interleukin 1-beta (IL-1 beta)-induced memory impairment. Modulation by alpha-melanocyte-stimulating hormone (alpha-MSH)

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Gonzalez, P. (author)

Molecular mechanisms involved in interleukin 1-beta (IL-1 beta)-induced memory impairment. Modulation by alpha-melanocyte-stimulating hormone (alpha-MSH)

Article/chapterEnglish2013

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Elsevier BV,2013
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LIBRIS-ID:oai:DiVA.org:uu-211006
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-211006URI
https://doi.org/10.1016/j.bbi.2013.08.007DOI

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype

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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.

Subject headings and genre

IL-1 beta
Memory consolidation
alpha-MSH
Glutamate release
p38
ERK
BDNF

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Machado, I. (author)
Vilcaes, A. (author)
Caruso, C. (author)
Roth, G. A. (author)
Schiöth, Helgi B.Uppsala universitet,Funktionell farmakologi(Swepub:uu)helgschi (author)
Lasaga, M. (author)
Scimonelli, T. (author)
Uppsala universitetFunktionell farmakologi (creator_code:org_t)

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In:Brain, behavior, and immunity: Elsevier BV34, s. 141-1500889-15911090-2139

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