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
Interleukin-1 beta-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and zif268 expression and alpha-melanocyte-stimulating hormone prevented these effects
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.
Show others and affiliations
2015 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 46, 137-146 p.Article in journal (Refereed) Published
Abstract [en]

The immune system is an important modulator of learning, memory and neural plasticity. Interleukin 1 13 (IL-1 beta), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies by our group have demonstrated that intrahippocampal administration of IL-1 beta impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (alpha-MSH). The mechanisms underlying the effect of IL-1 beta on memory reconsolidation have not yet been established. Therefore, we examined the effect of IL-1 beta on glutamate release, ERK phosphorylation and the activation of the transcription factor zinc finger- 268 (zif268) during reconsolidation. Our results demonstrated that IL-1 beta induced a significant decrease of glutamate release after reactivation of the fear memory and this effect was related to calcium concentration in hippocampal synaptosomes. IL-1 beta also reduced ERK phosphorylation and zif268 expression in the hippocampus. Central administration of a-MSH prevented the decrease in glutamate release, ERK phosphorylation and zif268 expression induced by IL-1 beta. Our results establish possible mechanisms involved in the detrimental effect of IL-1 beta on memory reconsolidation and also indicate that a-MSH may exert a beneficial modulatory role in preventing IL-1 beta effects.

Place, publisher, year, edition, pages
2015. Vol. 46, 137-146 p.
Keyword [en]
Interleukin-1 beta (IL-1 beta), Alpha-melanocyte-stimulating hormone (alpha-MSH), Memory reconsolidation, Glutamate release, zif268, ERK, Ca2+, Hippocampus
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:uu:diva-255266DOI: 10.1016/j.bbi.2015.01.012ISI: 000353751100018PubMedID: 25637483OAI: oai:DiVA.org:uu-255266DiVA: diva2:824839
Available from: 2015-06-22 Created: 2015-06-15 Last updated: 2017-12-04Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed

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
Immunology in the medical area

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 646 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