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An epigenetic mechanism for over-consolidation of fear memories
Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0002-0514-2628
Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Mahidol Univ, Thailand.
Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
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2022 (English)In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 27, no 12, p. 4893-4904Article in journal (Refereed) Published
Abstract [en]

Excessive fear is a hallmark of anxiety disorders, a major cause of disease burden worldwide. Substantial evidence supports a role of prefrontal cortex-amygdala circuits in the regulation of fear and anxiety, but the molecular mechanisms that regulate their activity remain poorly understood. Here, we show that downregulation of the histone methyltransferase PRDM2 in the dorsomedial prefrontal cortex enhances fear expression by modulating fear memory consolidation. We further show that Prdm2 knock-down (KD) in neurons that project from the dorsomedial prefrontal cortex to the basolateral amygdala (dmPFC-BLA) promotes increased fear expression. Prdm2 KD in the dmPFC-BLA circuit also resulted in increased expression of genes involved in synaptogenesis, suggesting that Prdm2 KD modulates consolidation of conditioned fear by modifying synaptic strength at dmPFC-BLA projection targets. Consistent with an enhanced synaptic efficacy, we found that dmPFC Prdm2 KD increased glutamatergic release probability in the BLA and increased the activity of BLA neurons in response to fear-associated cues. Together, our findings provide a new molecular mechanism for excessive fear responses, wherein PRDM2 modulates the dmPFC -BLA circuit through specific transcriptomic changes.

Place, publisher, year, edition, pages
Springer Nature , 2022. Vol. 27, no 12, p. 4893-4904
National Category
Neurosciences
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URN: urn:nbn:se:liu:diva-189083DOI: 10.1038/s41380-022-01758-6ISI: 000855637600001PubMedID: 36127428Scopus ID: 2-s2.0-85138397577OAI: oai:DiVA.org:liu-189083DiVA, id: diva2:1702577
Note

Funding Agencies|Swedish Research Council [2013-07434]; Region ostergotland; Stiftelsen Psykiatriska Forskningsfonden; Wallenberg Foundation; Knut och Alice Wallenberg Stiftelse Grant; Knut and Alice Wallenberg Foundation

Available from: 2022-10-11 Created: 2022-10-11 Last updated: 2023-03-20

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Barchiesi, RiccardoChanthongdee, KanatPetrella, MicheleXu, LiSöderholm, SimonDomi, EsiAugier, GaëlleCoppola, AndreaWiskerke, JoostSzczot, IlonaAugier, EricCantù, ClaudioHeilig, MarkusBarbier, Estelle
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Center for Social and Affective NeuroscienceFaculty of Medicine and Health SciencesDivision of Molecular Medicine and VirologyPsykiatriska kliniken i Linköping
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