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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd http://dublincore.org/schemas/xmls/qdc/dcterms.xsd"><dc:language>eng</dc:language><dc:creator>Spijker, Sabine</dc:creator><dc:creator>Koskinen, Maija-Kreetta</dc:creator><dc:creator>Riga, Danai</dc:creator><dc:title>Incubation of depression: ECM assembly and parvalbumin interneurons after stress.</dc:title><dc:subject>info:eu-repo/classification/ddc/610</dc:subject><dc:subject>Depression</dc:subject><dc:subject>Extracellular Matrix</dc:subject><dc:subject>Interneurons</dc:subject><dc:subject>Neurons</dc:subject><dc:subject>Parvalbumins</dc:subject><dc:subject>Chronic mild/unpredictable stress</dc:subject><dc:subject>Early life stress</dc:subject><dc:subject>Experience-dependent plasticity</dc:subject><dc:subject>Hippocampus</dc:subject><dc:subject>Hyper-excitability</dc:subject><dc:subject>Hypo-excitability</dc:subject><dc:subject>Prefrontal cortex</dc:subject><dc:subject>Restraint stress</dc:subject><dc:subject>Social defeat stress</dc:subject><dc:subject>Parvalbumins</dc:subject><dc:description>The extracellular space is occupied by a complex network of proteins creating a mesh-like assembly known as the extracellular matrix (ECM). ECM assembles into dense net-like structures, perineuronal nets (PNNs), that envelope cell somas and proximal neurites of predominantly parvalbumin+-(PV+) interneurons. ECM regulates cell-to-cell communication, thereby modulating neuronal network function. Accumulating evidence points to the importance of network dysfunction in the pathophysiology of psychiatric diseases, in which stress acts as a major predisposing factor. Here we review stress-induced changes in ECM/PNNs and PV+-interneurons in preclinical models of (or for) depression, with a special focus on social stress. We argue that the direction of these alterations largely depends on stress recency, as well as on stress timing and the brain region under investigation. A biphasic temporal regulation of ECM/PNNs and PV+-interneuron function is typically observed after stress. Understanding the complex mechanisms underlying ECM organization in relation to stress-induced molecular, cellular and network changes is crucial to further decipher the implications of ECM remodeling in the incubation of depressive symptoms.</dc:description><dc:source>Neuroscience &amp; biobehavioral reviews 118, 65 - 79 (2020). doi:10.1016/j.neubiorev.2020.07.015</dc:source><dc:type>info:eu-repo/semantics/article</dc:type><dc:type>info:eu-repo/semantics/publishedVersion</dc:type><dc:publisher>Elsevier Science</dc:publisher><dc:date>2020</dc:date><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:coverage>DE</dc:coverage><dc:identifier>https://pub.dzne.de/record/164427</dc:identifier><dc:identifier>https://pub.dzne.de/search?p=id:%22DZNE-2022-00979%22</dc:identifier><dc:audience>Researchers</dc:audience><dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neubiorev.2020.07.015</dc:relation><dc:relation>info:eu-repo/semantics/altIdentifier/issn/1873-7528</dc:relation><dc:relation>info:eu-repo/semantics/altIdentifier/issn/0149-7634</dc:relation><dc:relation>info:eu-repo/semantics/altIdentifier/pmid/pmid:32687884</dc:relation></oai_dc:dc>

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