Interleukin-1β-induced memory reconsolidation impairment is mediated by a reduction in glutamate release and zif268 expression and α-melanocyte-stimulating hormone prevented these effects
Autor: | Mercedes Lasaga, Patricia Verónica Gonzalez, Ivana Noelia Machado, Teresa Nieves Scimonelli, Lila Carniglia, Helgi B. Schiöth, Aldo Alejandro Vilcaes |
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Rok vydání: | 2015 |
Předmět: |
Male
MAPK/ERK pathway medicine.medical_specialty CIENCIAS MÉDICAS Y DE LA SALUD Melanocyte-stimulating hormone Neurociencias Interleukin-1beta Immunology Glutamic Acid Hippocampus Hippocampal formation Behavioral Neuroscience chemistry.chemical_compound Memory Internal medicine ALPHA-MELANOCYTE-STIMULATING HORMONE medicine Animals Phosphorylation Rats Wistar GLUTAMATE RELEASE Early Growth Response Protein 1 Memory Disorders Endocrine and Autonomic Systems Glutamate receptor Fear alpha-Melanocyte-stimulating hormone Rats ERK Ca2+ Medicina Básica Endocrinology chemistry alpha-MSH HIPPOCAMPUS Calcium Memory consolidation INTERLEUKIN 1 BETA zif268 Melanocortin MEMORY RECONSOLIDATION Synaptosomes |
Zdroj: | Brain, Behavior, and Immunity. 46:137-146 |
ISSN: | 0889-1591 |
Popis: | The immune system is an important modulator of learning, memory and neural plasticity. Interleukin 1β (IL-1β), a pro-inflammatory cytokine, significantly affects several cognitive processes. Previous studies by our group have demonstrated that intrahippocampal administration of IL-1β impairs reconsolidation of contextual fear memory. This effect was reversed by the melanocortin alpha-melanocyte-stimulating hormone (α-MSH). The mechanisms underlying the effect of IL-1β on memory reconsolidation have not yet been established. Therefore, we examined the effect of IL-1β on glutamate release, ERK phosphorylation and the activation of the transcription factor zinc finger- 268 (zif268) during reconsolidation. Our results demonstrated that IL-1β 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-1β also reduced ERK phosphorylation and zif268 expression in the hippocampus. Central administration of α-MSH prevented the decrease in glutamate release, ERK phosphorylation and zif268 expression induced by IL-1β. Our results establish possible mechanisms involved in the detrimental effect of IL-1β on memory reconsolidation and also indicate that α-MSH may exert a beneficial modulatory role in preventing IL-1β effects. Fil: Machado, Ivana Noelia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Instituto de Farmacología Experimental de Córdoba; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Farmacología; Argentina Fil: Gonzalez, Patricia Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Instituto de Farmacología Experimental de Córdoba; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Farmacología; Argentina Fil: Vilcaes, Aldo Alejandro. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (p); Argentina; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Quimica Biológica; Argentina Fil: Carniglia, Lila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina Fil: Schiöth, Helgi B.. Uppsala University; Suecia Fil: Lasaga, Mercedes Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; Argentina; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina Fil: Scimonelli, Teresa Nieves. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Instituto de Farmacología Experimental de Córdoba; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Farmacología; Argentina |
Databáze: | OpenAIRE |
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