Glucocorticoid receptor signaling in astrocytes is required for aversive memory formation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Magdalena Tertil, Urszula Skupio, Justyna Barut, Valentyna Dubovyk, Agnieszka Wawrzczak-Bargiela, Zbigniew Soltys, Slawomir Golda, Lucja Kudla, Lucja Wiktorowska, Klaudia Szklarczyk, Michal Korostynski, Ryszard Przewlocki, Michal Slezak

ABSTRACT

Stress elicits the release of glucocorticoids (GCs) that regulate energy metabolism and play a role in emotional memory. Astrocytes express glucocorticoid receptors (GR), but their contribution to cognitive effects of GC's action in the brain is unknown. To address this question, we studied how astrocyte-specific elimination of GR affects animal behavior known to be regulated by stress. Mice with astrocyte-specific ablation of GR presented impaired aversive memory expression in two different paradigms of Pavlovian learning: contextual fear conditioning and conditioned place aversion. These mice also displayed compromised regulation of genes encoding key elements of the glucose metabolism pathway upon GR stimulation. In particular, we identified that the glial, but not the neuronal isoform of a crucial stress-response molecule, Sgk1, undergoes GR-dependent regulation in vivo and demonstrated the involvement of SGK1 in regulation of glucose uptake in astrocytes. Together, our results reveal astrocytes as a central element in GC-dependent formation of aversive memory and suggest their relevance for stress-induced alteration of brain glucose metabolism. Consequently, astrocytes should be considered as a cellular target of therapies of stress-induced brain diseases. More... »

PAGES

255

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41398-018-0300-x

    DOI

    http://dx.doi.org/10.1038/s41398-018-0300-x

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1110255698

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30487639


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