GSTDTAP  > 气候变化
DOI10.1126/science.abf4646
Bespoke myelin tailored to neuron type
Belgin Yalçın; Michelle Monje
2020-12-18
发表期刊Science
出版年2020
英文摘要Myelin is a critical component of nervous system form and function. This compact lipid-rich membrane, generated by oligodendrocytes, wraps around axons to provide metabolic support and enable rapid signal conduction. Small changes in the number or geometric parameters of myelin sheaths can powerfully modulate the speed of action potential conduction, thereby influencing neural circuit dynamics and coordinated circuit function. Initially considered to be largely established during postnatal nervous system development, it is increasingly appreciated that myelination continues throughout adulthood ([ 1 ][1]–[ 3 ][2]) in mice and humans. Notably, in the adult neocortex, ample unmyelinated territory and discontinuously myelinated cortical axons ([ 4 ][3]) provide a substrate for substantial tuning of circuit function. On page 1437 of this issue, Yang et al. ([ 5 ][4]) introduce the principle that experience differentially regulates myelin plasticity in distinct neuron classes in the neocortex, indicating that experience may fine tune neuronal circuit function. Myelination in the neocortex and certain white matter tracts can occur in a manner that is regulated by experience and neuronal activity ([ 2 ][5], [ 3 ][2], [ 6 ][6], [ 7 ][7]). These experience- and activity-dependent changes in myelin represent both de novo myelin by new oligodendrocytes and myelin remodeling by existing oligodendrocytes ([ 3 ][2], [ 8 ][8]). The relative contribution of existing versus new oligodendrocytes may vary across different anatomical regions. This plasticity of myelin is adaptive in the healthy nervous system, where these changes promote coordinated circuit function ([ 6 ][6], [ 9 ][9], [ 10 ][10]) and contribute to neurological functions including motor performance, learning, and memory ([ 2 ][5], [ 6 ][6], [ 7 ][7], [ 11 ][11], [ 12 ][12]). ![Figure][13] Experience-dependent myelin remodeling Myelin profiles of excitatory callosal projection neurons (CPNs) and inhibitory parvalbumin-expressing γ-aminobutyric acid–mediated (GABAergic) interneurons (PV-INs) in the superficial visual cortex vary according to visual experience. Monocular deprivation alters myelin remodeling differently in these two distinct neuron classes of the neocortex: Myelination of CPNs is not altered, whereas PV-INs initially exhibit increased elongation, followed by contraction of preexisting myelin sheaths. Consequently, ion channels along the PV-IN axon are redistributed. These changes could alter circuit dynamics to adapt to monocular vision. GRAPHIC: KELLIE HOLOSKI/ SCIENCE For plasticity of myelin to confer the subtle changes that adaptively tune circuit function, precision is required. Concordantly, activity-regulated myelin changes are unlikely to occur uniformly in the nervous system. For example, intrinsic differences exist in the myelin profiles generated by oligodendrocytes from different regions of the mouse central nervous system ([ 13 ][14]), and individual oligodendrocytes preferentially myelinate inhibitory or excitatory neurons ([ 14 ][15]). Stimulation of premotor cortex neurons in mice induces myelination in the axons of callosal projection neurons, but not in the axons of corticospinal projection neurons ([ 2 ][5]), suggesting diversity in the activity-regulated myelin response. But it has not been clear whether this difference reflects regional heterogeneity in oligodendrocytes and their precursors or differences in these subpopulations of neurons. Yang et al. used longitudinal in vivo imaging of fluorescently labeled excitatory callosal projection neurons (CPNs), parvalbumin-expressing interneurons (PV-INs) that release the neurotransmitter γ-aminobutyric acid (GABA), and oligodendrocytes in the superficial primary visual cortex of young adult mice during normal visual experience and during monocular deprivation. Only a fraction of CPNs in young adult mice with normal visual experience were myelinated compared to most PV-INs, indicating that these two neuron classes exhibit different temporal patterns of postnatal myelination. Initial tracking of myelin dynamics revealed that the average myelin segment is longer on PV-INs compared to CPNs. Myelin remodeling can involve myelin sheath elongation and contraction along the axon, and these elongation and contraction events were found to balance each other such that the total myelination of PV-IN axons remains stable with normal visual experience. For CPN axons, the predominance of elongation events of individual myelin segments increases myelination over time, which is consistent with the protracted myelination of these neurons during adulthood. Myelin segments produced by newly generated oligodendrocytes were rare in the superficial visual cortex, but de novo myelin sheaths display more dynamic remodeling in comparison to preexisting myelin segments. Monocular deprivation is a well-characterized model of altered sensory experience known to induce plasticity in the response properties of inhibitory and excitatory neurons and to elicit reconfiguration of the visual system ([ 15 ][16]). After 14 days of monocular deprivation, CPN myelin sheath dynamics remained unchanged, indicating that monocular deprivation does not affect myelin plasticity of CPNs in the superficial visual cortex. By contrast, increased myelin sheath remodeling was observed on axons of visual cortex PV-INs. Thus, experience-regulated reconfiguration of the visual system after monocular deprivation drives neuron-class–specific myelin remodeling in the neocortex. Like the neuronal alterations that monocular deprivation induces—the dendritic arbors of neurons initially retract and subsequently elongate—myelin remodeling also follows a temporally defined pattern. In the first phase after initiation of monocular deprivation, preexisting myelin sheaths display an increased elongation rate, and subsequently elongation events return to baseline. In the second phase, there is an increased contraction rate of other sets of stable sheaths. During these remodeling stages, existing oligodendrocytes are also recruited to generate new myelin on PV-IN axons (see the figure). Myelin segments on an axon determine the localization of nodes of Ranvier and the distribution of ion channels, which are involved in action potential propagation along the axon. As a result of myelin changes on PV-IN axons after monocular deprivation, these ion channel clusters at nodes of Ranvier are also redistributed. Reorganization of axonal branching is also observed with monocular deprivation; however, myelin remodeling is restricted to the stable axonal branches of PV-INs. Evidently, myelin alterations are not a downstream event of axonal rearrangements after monocular deprivation but rather another level of plasticity. Small changes in myelination can result in profound alterations to circuit dynamics and contribute critically to achieving neuronal oscillations and coordinating precise spike-time arrival to common targets ([ 6 ][6], [ 9 ][9], [ 10 ][10]); with consequent effects on overall circuit function. Precise regulation of experience and activity-regulated changes in myelin are required to be adaptive rather than maladaptive. The study by Yang et al. begins to elucidate principles of neuron-class–specific diversification of myelin plasticity. Future work will continue to elucidate how various classes of neurons in diverse anatomical regions interact with oligodendrocyte lineage cells to regulate de novo myelination or myelin remodeling in response to activity and experience. The molecular mechanisms that mediate the neuron-glial interactions that underlie myelin plasticity may be similarly diverse and potentially neuron-class specific. A systems-level understanding of myelin plasticity will be necessary to elucidate how differential myelin adjustments within neural circuits affect behavior in the healthy nervous system, and how aberrations in these powerful mechanisms of plasticity may contribute to neurological and neuropsychiatric diseases. 1. [↵][17]1. K. Young et al ., Neuron 77, 873 (2013). [OpenUrl][18][CrossRef][19][PubMed][20][Web of Science][21] 2. [↵][22]1. E. M. Gibson et al ., Science 344, 1252304 (2014). [OpenUrl][23][Abstract/FREE Full Text][24] 3. [↵][25]1. E. G. Hughes et al ., Nat. 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领域气候变化 ; 资源环境
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专题气候变化
资源环境科学
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Belgin Yalçın,Michelle Monje. Bespoke myelin tailored to neuron type[J]. Science,2020.
APA Belgin Yalçın,&Michelle Monje.(2020).Bespoke myelin tailored to neuron type.Science.
MLA Belgin Yalçın,et al."Bespoke myelin tailored to neuron type".Science (2020).
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