TY - JOUR
T1 - Incubation of depression
T2 - ECM assembly and parvalbumin interneurons after stress
AU - Spijker, Sabine
AU - Koskinen, Maija Kreetta
AU - Riga, Danai
PY - 2020/11
Y1 - 2020/11
N2 - 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.
AB - 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.
KW - Chronic mild/unpredictable stress
KW - Early life stress
KW - Experience-dependent plasticity
KW - Hippocampus
KW - Hyper-excitability
KW - Hypo-excitability
KW - Prefrontal cortex
KW - Restraint stress
KW - Social defeat stress
UR - http://www.scopus.com/inward/record.url?scp=85088626218&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85088626218&partnerID=8YFLogxK
U2 - 10.1016/j.neubiorev.2020.07.015
DO - 10.1016/j.neubiorev.2020.07.015
M3 - Review article
C2 - 32687884
AN - SCOPUS:85088626218
VL - 118
SP - 65
EP - 79
JO - Neuroscience and Biobehavioral Reviews
JF - Neuroscience and Biobehavioral Reviews
SN - 0149-7634
ER -