Genetic Control of Myelin Plasticity after Chronic Psychosocial Stress

Laine, Mikaela; Trontti, Kalevi; Misiewicz, Zuzanna; Sokołowska, Ewa; Kulesskaya, Natalia; Heikkinen, Aino; Saarnio, Suvi; Balcells, Ingrid; Ameslon, Pierre; Greco, Dario; Mattila, Pirkko; Ellonen, Pekka; Paulín, Lars; Auvinen, Petri; Jokitalo, Eija; Hovatta, Iiris

doi:10.1523/eneuro.0166-18.2018

Cited by 54 publications

(135 citation statements)

References 82 publications

(86 reference statements)

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“…Of note, these stress‐related transcriptional changes were consistently associated with modifications in myelin thickness in some specific regions (e.g., medial prefrontal cortex, ventral hippocampus, etc.) (Laine et al, ). In other studies, different types of chronic stress such as repeated water immersion and restraint stress led to structural modifications of the oligodendrocytes in mice.…”

Section: Sleep and Myelinmentioning

confidence: 99%

“…Another possibility is that the effects of sleep loss on myelin are mediated by the behavioral stress inherently associated with sleep loss. In this regard, several myelin‐related transcripts have been found to be downregulated by psychosocial stress, a chronic behavioral stress that in mice is usually modeled by the chronic social defeat stress paradigm (Laine et al, ). Of note, these stress‐related transcriptional changes were consistently associated with modifications in myelin thickness in some specific regions (e.g., medial prefrontal cortex, ventral hippocampus, etc.)…”

Section: Sleep and Myelinmentioning

confidence: 99%

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The role of sleep and wakefulness in myelin plasticity

Vivo

Bellesi

2019

Glia

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Myelin plasticity is gaining increasing recognition as an essential partner to synaptic plasticity, which mediates experience‐dependent brain structure and function. However, how neural activity induces adaptive myelination and which mechanisms are involved remain open questions. More than two decades of transcriptomic studies in rodents have revealed that hundreds of brain transcripts change their expression in relation to the sleep–wake cycle. These studies consistently report upregulation of myelin‐related genes during sleep, suggesting that sleep represents a window of opportunity during which myelination occurs. In this review, we summarize recent molecular and morphological studies detailing the dependence of myelin dynamics after sleep, wake, and chronic sleep loss, a condition that can affect myelin substantially. We present novel data about the effects of sleep loss on the node of Ranvier length and provide a hypothetical mechanism through which myelin changes in response to sleep loss. Finally, we discuss the current findings in humans, which appear to confirm the important role of sleep in promoting white matter integrity.

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Section: Sleep and Myelinmentioning

confidence: 99%

Section: Sleep and Myelinmentioning

confidence: 99%

The role of sleep and wakefulness in myelin plasticity

Vivo

Bellesi

2019

Glia

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“…previously [26]. FST was also used as a stressor before measurement of blood corticosterone levels, thus 30 min after the test mice were anesthetized with 4% isoflurane and blood samples were collected from the submandibular vein.…”

Section: Open Field (Of) Forced Swim (Fst) and Elevated Zero Maze (mentioning

confidence: 99%

Kainate receptor auxiliary subunit NETO2 is required for normal fear expression and extinction

Mennesson

Rydgren

Lipina

et al. 2019

Neuropsychopharmacol.

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NETO1 and NETO2 are auxiliary subunits of kainate receptors (KARs). They interact with native KAR subunits to modulate multiple aspects of receptor function. Variation in KAR genes has been associated with psychiatric disorders in humans, and in mice, knockouts of the Grik1 gene have increased, while Grik2 and Grik4 knockouts have reduced anxiety-like behavior. To determine whether the NETO proteins regulate anxiety and fear through modulation of KARs, we undertook a comprehensive behavioral analysis of adult Neto1-/and Neto2-/mice. We observed no differences in anxiety-like behavior. However, in cued fear conditioning, Neto2-/-, but not Neto1-/mice, showed higher fear expression and delayed extinction compared to wild type mice. We established, by in situ hybridization, that Neto2 was expressed in both excitatory and inhibitory neurons throughout the fear circuit including the medial prefrontal cortex, amygdala, and hippocampus. Finally, we demonstrated that the relative amount of synaptosomal KAR GLUK2/3 subunit was 20.8% lower in the ventral hippocampus and 36.5% lower in the medial prefrontal cortex in Neto2-/compared to the Neto2 +/+ mice. The GLUK5 subunit abundance was reduced 23.8% in the ventral hippocampus and 16.9% in the amygdala. We conclude that Neto2 regulates fear expression and extinction in mice, and that its absence increases conditionability, a phenotype related to posttraumatic stress disorder and propose that this phenotype is mediated by reduced KAR subunit abundance at synapses of fear-associated brain regions.

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“…0.05) and were analyzed using mixed ANOVA, generalized estimating equation (GEE), or Kolmogorov-Smirnov tests (Table 1). GEE analysis was used to control for within-subject dependencies of individual data points collected from the same animal (e.g., neurons recorded from slices originating from the same mouse) or from the same cell/image (e.g., PV cell intensities measured from the same image), as previously described (Hanley et al, 2003;Laine et al, 2018). Statistical analyses were conducted using SPSS Statistics 24 (IBM), GraphPad Prism7 (GraphPad Software), or RStudio (RStudio Inc.).…”

Section: Discussionmentioning

confidence: 99%

Kainate Receptor Auxiliary Subunit NETO2-Related Cued Fear Conditioning Impairments Associate with Defects in Amygdala Development and Excitability

Mennesson

Orav

Gigliotta

et al. 2020

eNeuro

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NETO2 is an auxiliary subunit for kainate-type glutamate receptors that mediate normal cued fear expression and extinction. Since the amygdala is critical for these functions, we asked whether Neto2 À/À mice have compromised amygdala function. We measured the abundance of molecular markers of neuronal maturation and plasticity, parvalbumin-positive (PV 1), perineuronal net-positive (PNN 1), and double positive (PV 1 PNN 1) cells

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Genetic Control of Myelin Plasticity after Chronic Psychosocial Stress

Abstract: Visual Abstract

Cited by 54 publications

References 82 publications

The role of sleep and wakefulness in myelin plasticity

The role of sleep and wakefulness in myelin plasticity

Kainate receptor auxiliary subunit NETO2 is required for normal fear expression and extinction

Kainate Receptor Auxiliary Subunit NETO2-Related Cued Fear Conditioning Impairments Associate with Defects in Amygdala Development and Excitability

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