iPlasticity : Induced juvenile-like plasticity in the adult brain as a mechanism of antidepressants

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Umemori , J , Winkel , F , Didio , G , Pou , M L & Castren , E 2018 , ' iPlasticity : Induced juvenile-like plasticity in the adult brain as a mechanism of antidepressants ' , Psychiatry and Clinical Neurosciences , vol. 72 , no. 9 , pp. 633-653 . https://doi.org/10.1111/pcn.12683

Title: iPlasticity : Induced juvenile-like plasticity in the adult brain as a mechanism of antidepressants
Author: Umemori, Juzoh; Winkel, Frederike; Didio, Giuliano; Pou, Maria Llach; Castren, Eero
Contributor: University of Helsinki, Neuroscience Center
University of Helsinki, Neuroscience Center
University of Helsinki, Neuroscience Center
University of Helsinki, Neuroscience Center
Date: 2018-09
Language: eng
Number of pages: 21
Belongs to series: Psychiatry and Clinical Neurosciences
ISSN: 1323-1316
URI: http://hdl.handle.net/10138/252769
Abstract: The network hypothesis of depression proposes that mood disorders reflect problems in information processing within particular neural networks. Antidepressants (AD), including selective serotonin reuptake inhibitors (SSRI), function by gradually improving information processing within these networks. AD have been shown to induce a state of juvenile-like plasticity comparable to that observed during developmental critical periods: Such critical-period-like plasticity allows brain networks to better adapt to extrinsic and intrinsic signals. We have coined this drug-induced state of juvenile-like plasticity iPlasticity.' A combination of iPlasticity induced by chronic SSRI treatment together with training, rehabilitation, or psychotherapy improves symptoms of neuropsychiatric disorders and issues underlying the developmentally or genetically malfunctioning networks. We have proposed that iPlasticity might be a critical component of AD action. We have demonstrated that iPlasticity occurs in the visual cortex, fear erasure network, extinction of aggression caused by social isolation, and spatial reversal memory in rodent models. Chronic SSRI treatment is known to promote neurogenesis and to cause dematuration of granule cells in the dentate gyrus and of interneurons, especially parvalbumin interneurons enwrapped by perineuronal nets in the prefrontal cortex, visual cortex, and amygdala. Brain-derived neurotrophic factor (BDNF), via its receptor tropomyosin kinase receptor B, is involved in the processes of synaptic plasticity, including neurogenesis, neuronal differentiation, weight of synapses, and gene regulation of synaptic formation. BDNF can be activated by both chronic SSRI treatment and neuronal activity. Accordingly, the BDNF/tropomyosin kinase receptor B pathway is critical for iPlasticity, but further analyses will be needed to provide mechanical insight into the processes of iPlasticity.
Subject: brain-derived neurotrophic factor
tropomyosin kinase receptor B
dematuration
neurogenesis
neuronal plasticity
parvalbumin
perineuronal nets
CHRONIC FLUOXETINE TREATMENT
OCULAR DOMINANCE PLASTICITY
MEDIAL PREFRONTAL CORTEX
LONG-TERM POTENTIATION
FACTOR MESSENGER-RNA
NERVE GROWTH-FACTOR
CHRONIC ELECTROCONVULSIVE SEIZURES
HIPPOCAMPAL CELL-PROLIFERATION
NEUROTROPHIC FACTOR RECEPTORS
ENHANCED SYNAPTIC PLASTICITY
3112 Neurosciences
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