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IL-1 beta reduces GluAl phosphorylation and its surface expression during memory reconsolidation and cc-melanocyte-stimulating hormone can modulate these effects
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology. Univ Nacl Cordoba, Fac Ciencias Quim, Dept Farmacol, IFEC CONICET, Cordoba, Argentina..
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Functional Pharmacology.ORCID iD: 0000-0001-7112-0921
UBA CONICET, Fac Med, Inst Invest Biomed INBIOMED, Buenos Aires, DE, Argentina..
Univ Nacl Cordoba, Fac Ciencias Quim, Dept Farmacol, IFEC CONICET, Cordoba, Argentina..
2018 (English)In: Neuropharmacology, ISSN 0028-3908, E-ISSN 1873-7064, Vol. 128, p. 314-323Article in journal (Refereed) Published
Abstract [en]

Pro-inflammatory cytokines can affect cognitive processes such as learning and memory. Particularly, interleukin-beta (IL-beta) influences hippocampus-dependent memories. We previously reported that administration of IL-1 beta in dorsal hippocampus impaired contextual fear memory reconsolidation. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (a-MSH). Our results also demonstrated that IL-1 beta produced a significant decrease in glutamate release from dorsal hippo campus synaptosomes after reactivation of the fear memory. Therefore, we investigated whether IL-beta administration can affect GIuA1 AMPA subunit phosphorylation, surface expression, and total expression during reconsolidation of a contextual fear memory. Also, we studied the modulatory effect of alpha-MSH. We found that IL-beta reduced phosphorylation of this subunit at Serine 831 and Serine 845 60 min after contextual fear memory reactivation. The intrahippocampal administration of IL-beta after memory reactivation also induced a decrease in surface expression and total expression of GIuA1. alpha-MSH prevented the effect of IL-beta on GIuAI phosphorylation in Serine 845, but not in Serine 831. Moreover, treatment with alpha-MSH also prevented the effect of the cytokine on GluAl surface and total expression after memory reactivation. Our results demonstrated that IL-beta regulates phosphorylation of GIuAI and may thus play an important role in modulation of AMPAR function and synaptic plasticity in the brain. These findings further illustrate the importance of IL-beta in cognition processes dependent on the hippocampus, and also reinforced the fact that alpha-MSH can reverse IL-1 beta effects on memory reconsolidation. (C) 2017 Elsevier Ltd. All rights reserved.

Place, publisher, year, edition, pages
Elsevier, 2018. Vol. 128, p. 314-323
Keywords [en]
Interleukin-1-beta (IL-1 beta), Alpha-melanocyte-stimulating hormone (alpha-MSH), Memory reconsolidation, AMPA, GluAl, p-Ser831 GluA1, p-Ser845 GIuA1, Hippocampus
National Category
Neurology
Identifiers
URN: urn:nbn:se:uu:diva-340457DOI: 10.1016/j.neuropharm.2017.09.041ISI: 000418977200028PubMedID: 29042315OAI: oai:DiVA.org:uu-340457DiVA, id: diva2:1183120
Available from: 2018-02-15 Created: 2018-02-15 Last updated: 2018-02-19Bibliographically approved

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Schiöth, Helgi B.

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