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Review
. 2019 Nov;67(11):2142-2152.
doi: 10.1002/glia.23667. Epub 2019 Jun 25.

The role of sleep and wakefulness in myelin plasticity

Luisa de Vivo  1 , Michele Bellesi  1
Affiliations
Review

The role of sleep and wakefulness in myelin plasticity

Luisa de Vivo et al. Glia. 2019 Nov.

Abstract

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.

Keywords: brain; myelin; oligodendrocyte; sleep deprivation; white matter.

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Conflict of interest statement

The authors have no conflict of interest to declare.

Figures

Figure 1
Figure 1
Sleep and myelin. (a). Heat diagram showing the expression intensity of differentially expressed transcripts of oligodendrocyte‐enriched forebrain samples of sleeping (S), awake (W), sleep deprived (SD). (b). Left, example of proliferating OPCs stained by the specific marker PDGFRα (green) and positive for BrdU (red). Scale bar: 15 μm. Right, scheme describing the experiment design (top) and quantification of proliferating OPCs in the cerebral cortex of mice after 8 hr of S, W, and SD (bottom). Adapted from Bellesi et al., 2013, 2015
Figure 2
Figure 2
Myelin changes after chronic sleep loss. Top row: Distribution of g‐ratio, axon diameter, and myelin thickness measurements in adolescent mice after sleep (S), acute sleep deprivation (SD), chronic sleep restriction (CSR: ~5 days), recovery sleep (RS: 32 hr after the end of ~5 days of CSR). For axon diameter and myelin thickness, a log transformation has been applied to raw values, so the units are log(μm). Bottom row: Representative corpus callosum coronal section at the level of the decussation of the anterior commissure (+0.14 mm a/P from bregma) depicting YFP+ fibers (blue) and CASPR+ puncta (yellow). Red arrows indicate examples of nodes considered for the internodal length analysis, which are shown at larger magnification in the squared boxes. The red line along the axon indicates the internodal length, while the green arrows indicate node length. In the bottom scheme, representative nodes of Ranvier with paranodal sites (yellow) and the red line representing the internodal length are depicted. Graphs indicate distribution of internodal and node lengths values from the corpus callosum of S (n = 4 mice, 173 internodes and 1,412 nodes), SD (n = 4 mice, 180 internodes and 1,310 nodes), and CSR (n = 7 mice, 316 internodes and 2006 nodes) mice. Note that node length has been estimated as the shortest distance between two closely apposed CASPR+ puncta along the YFP+ axon. Data were analysed with ANOVA followed by Bonferroni's post hoc test. Adapted from Bellesi et al., 2018
Figure 3
Figure 3
How myelin is remodelled by chronic sleep loss. A scheme representing the hypothetical mechanism underpinning node length widening and myelin thinning. As the chronic sleep restriction progresses, the outer paranodal loops (dashed thin arrows) first detach form the paranodal region, thus increasing the node length, and then retract into the oligodendrocyte with consequent myelin sheath thinning (dashed thick arrows)
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