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5. Oligodendrocyte Dynamics in the Healthy Adult CNS: Evidence for Myelin Remodeling

Author

Young, Kaylene M., Psachoulia, Konstantina, Tripathi, Richa B., Dunn, Sara-Jane, Cossell, Lee, Attwell, David, Tohyama, Koujiro, and Richardson, William D.

Subjects
Central Nervous System, Aging, Microscopy, Confocal, Receptor, Platelet-Derived Growth Factor alpha, Cell Survival, Neuroscience(all), Cell Cycle, Cell Count, Cell Differentiation, Mice, Transgenic, Optic Nerve, Immunohistochemistry, Polymerase Chain Reaction, Article, Mice, Oligodendroglia, nervous system, Animals, Microscopy, Immunoelectron, Cell Division, Myelin Sheath
Abstract

Summary Oligodendrocyte precursors (OPs) continue to proliferate and generate myelinating oligodendrocytes (OLs) well into adulthood. It is not known whether adult-born OLs ensheath previously unmyelinated axons or remodel existing myelin. We quantified OP division and OL production in different regions of the adult mouse CNS including the 4-month-old optic nerve, in which practically all axons are already myelinated. Even there, all OPs were dividing and generating new OLs and myelin at a rate higher than can be explained by first-time myelination of naked axons. We conclude that adult-born OLs in the optic nerve are engaged in myelin remodeling, either replacing OLs that die in service or intercalating among existing myelin sheaths. The latter would predict that average internode length should decrease with age. Consistent with that, we found that adult-born OLs elaborated much shorter but many more internodes than OLs generated during early postnatal life., Highlights ► Quanitification of oligodendrocyte (OL) and myelin production in the adult mouse CNS ► OLs are made even in the optic nerve, where nearly all axons are already myelinated ► Adult-born OLs in the optic nerve appear to engage in myelin remodeling, It is not known whether adult-born oligodendrocytes ensheath previously unmyelinated axons or remodel existing myelin. In this study, Young et al. find evidence for myelin remodeling by adult-born oligodendrocytes in the optic nerve.

Published
2013

12. Synaptic Energy Use and Supply

Author

Harris, Julia J., Jolivet, Renaud, and Attwell, David

Subjects
*NEUROPHYSIOLOGY, *SYNAPSES, *BIOENERGETICS, *NEURAL transmission, *ENERGY consumption, *ADENOSINE triphosphate
Abstract

Neuronal computation is energetically expensive. Consequently, the brain’s limited energy supply imposes constraints on its information processing capability. Most brain energy is used on synaptic transmission, making it important to understand how energy is provided to and used by synapses. We describe how information transmission through presynaptic terminals and postsynaptic spines is related to their energy consumption, assess which mechanisms normally ensure an adequate supply of ATP to these structures, consider the influence of synaptic plasticity and changing brain state on synaptic energy use, and explain how disruption of the energy supply to synapses leads to neuropathology. [ABSTRACT FROM AUTHOR]

Published
2012
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13. Microglial Ramification, Surveillance, and Interleukin-1β Release Are Regulated by the Two-Pore Domain K + Channel THIK-1.

Author

Madry C, Kyrargyri V, Arancibia-Cárcamo IL, Jolivet R, Kohsaka S, Bryan RM, and Attwell D

Subjects
Adenosine Triphosphate pharmacology, Animals, Cell Movement, Cell Polarity, Cell Shape, Cell Surface Extensions physiology, Chemotaxis physiology, Inflammasomes metabolism, Membrane Potentials, Mice, Mice, Knockout, Microglia drug effects, Potassium physiology, Potassium Channels, Tandem Pore Domain antagonists & inhibitors, Potassium Channels, Tandem Pore Domain deficiency, Rats, Rats, Sprague-Dawley, Receptors, Purinergic P2Y12 physiology, Transcriptome, Interleukin-1beta physiology, Microglia physiology, Potassium Channels, Tandem Pore Domain physiology
Abstract

Microglia exhibit two modes of motility: they constantly extend and retract their processes to survey the brain, but they also send out targeted processes to envelop sites of tissue damage. We now show that these motility modes differ mechanistically. We identify the two-pore domain channel THIK-1 as the main K + channel expressed in microglia in situ. THIK-1 is tonically active, and its activity is potentiated by P2Y 12 receptors. Inhibiting THIK-1 function pharmacologically or by gene knockout depolarizes microglia, which decreases microglial ramification and thus reduces surveillance, whereas blocking P2Y 12 receptors does not affect membrane potential, ramification, or surveillance. In contrast, process outgrowth to damaged tissue requires P2Y 12 receptor activation but is unaffected by blocking THIK-1. Block of THIK-1 function also inhibits release of the pro-inflammatory cytokine interleukin-1β from activated microglia, consistent with K + loss being needed for inflammasome assembly. Thus, microglial immune surveillance and cytokine release require THIK-1 channel activity., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2018
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