Neuroglial interactions underpinning myelin plasticity

Abstract

The CNS is extremely responsive to an ever-changing environment. Studies of neural circuit plasticity focus almost exclusively on functional and structural changes of neuronal synapses. In recent years, however, myelin plasticity has emerged as a potential modulator of neuronal networks. Myelination of previously unmyelinated axons and changes in the structure of myelin on already-myelinated axons (similar to changes in internode number and length or myelin thickness or geometry of the nodal area) can in theory have significant effects on the function of neuronal networks. In this article, the authors review the current evidence for myelin changes occurring in the adult CNS, highlight some potential underlying mechanisms of how neuronal activity may regulate myelin changes, and explore the similarities between neuronal and myelin plasticity. © 2017 Wiley Periodicals, Inc. Develop Neurobiol 78: 93-107, 2018.

A moment of change: shifts in myeloarchitecture characterise adolescent development of cortical gradients

“…While both sets of agerelated changes were strongly and preferentially located in heteromodal and unimodal association cortex, they only partially overlapped which was also supported by gene expression analysis. Indeed, only skewness but not mean myelin changes were driven by oligodendrocyte modulation 24 , and these effects were found to be independent from interface blurring and cortical thickness. A recent review 24 proposed mechanisms of experience-dependent myelination, which appear to align with our findings.…”

“…Indeed, only skewness but not mean myelin changes were driven by oligodendrocyte modulation 24 , and these effects were found to be independent from interface blurring and cortical thickness. A recent review 24 proposed mechanisms of experience-dependent myelination, which appear to align with our findings. Accordingly, increasing mean likely reflects myelination of previously unmyelinated axons.…”

“…Such a sensory-fugal gradient was previously described by Mesulam 15 based on nonhuman primate research to encapsulate cortex-wide variations in architecture and connectivity, and has since been suggested to reflect increasing synaptic plasticity towards transmodal regions 52 . Systematic variations in the degree of experience-dependent plasticity may explain why myelin-derived markers develop differently along the sensory-fugal gradient 24 , in contrast to other known developmental gradients such as the rostro-caudal timing of terminal neurogenesis 53 . Differentiation of association cortices also conforms with notions of the "tethering hypothesis" of cortical evolution 54 .…”

The fate and function of oligodendrocyte progenitor cells after traumatic spinal cord injury

“…Additionally, OPCs also form close connections with neurons which allow them to monitor changes in neuronal activity (Bergles, Roberts, Somogyi, & Jahr, 2000;Gallo, Mangin, Kukley, & Dietrich, 2008;Hill et al, 2014;Hughes et al, 2013). These connections have properties similar to traditional neuron-neuron synapses, including accumulation of vesicles in presynaptic terminals apposed from OPCs, expression of neurotransmitter receptors on OPCs akin to postsynaptic neurons, release of vesicles into the intersynaptic space, and subsequent fast-kinetic currents in OPCs (Bergles et al, 2000;Gallo et al, 1996;Hamilton et al, 2017;Karadottir, Hamilton, Bakiri, & Attwell, 2008;Kukley, Capetillo-Zarate, & Dietrich, 2007;Ziskin, Nishiyama, Rubio, Fukaya, & Bergles, 2007), and has been thoroughly reviewed elsewhere (Almeida & Lyons, 2014;Bergles, Jabs, & Steinhauser, 2010;de Faria Jr., Pama, Evans, Luzhynskaya, & Karadottir, 2018). In parallel to development where OPCs have synaptic input from unmyelinated axons (Kukley et al, 2007;Ziskin et al, 2007), demyelination increases excitatory currents within OPCs, which are suppressed by the administration of tetrodotoxin (a voltage-gated sodium channel blocker) to block neuronal activity (Gautier et al, 2015).…”

The oligodendrocyte growth cone and its actin cytoskeleton: A fundamental element for progenitor cell migration and CNS myelination

“…Within the past few years, it has been recognized that myelination likely follows a basic intrinsic program that functions in the absence of extrinsic molecular instruction. This intrinsic program is thought to be modulated by a so‐called “adaptive program” initiated by extrinsic molecular signals and/or axonal electrical activity (Bechler, Byrne, & Ffrench‐Constant, ; Bechler, Swire, & Ffrench‐Constant, ; de Faria Jr., Pama, Evans, Luzhynskaya, & Karadottir, ; Foster, Bujalka, & Emery, ; Gibson, Geraghty, & Monje, ). Thus, the regulation of myelination via the action of extracellular factors, here referred to as “extrinsically modulated myelination,” could be considered a form of “adaptive” myelination.…”