uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Molecular mechanisms involved in interleukin 1-beta (IL-1 beta)-induced memory impairment. Modulation by alpha-melanocyte-stimulating hormone (alpha-MSH)
Show others and affiliations
2013 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 34, 141-150 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2013. Vol. 34, 141-150 p.
Keyword [en]
IL-1 beta, Memory consolidation, alpha-MSH, Glutamate release, p38, ERK, BDNF
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-211006DOI: 10.1016/j.bbi.2013.08.007ISI: 000325840300017OAI: oai:DiVA.org:uu-211006DiVA: diva2:665527
Available from: 2013-11-20 Created: 2013-11-19 Last updated: 2017-12-06Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text

Authority records BETA

Schiöth, Helgi B.

Search in DiVA

By author/editor
Schiöth, Helgi B.
By organisation
Functional Pharmacology
In the same journal
Brain, behavior, and immunity
Medical and Health Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 622 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf