Oligodendroglia-lineage cells in brain plasticity, homeostasis and psychiatric disorders

Birey, Fikri; Kokkosis, Alexandros G.; Aguirre, Adán

doi:10.1016/j.conb.2017.09.016

Cited by 40 publications

(31 citation statements)

References 133 publications

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“…Myelin is a fundamental cellular structure in the vertebrate nervous system, and its precise formation and regulation are critical for complex neuronal function, including cognition 1,2 . The importance of myelin for circuit function is made apparent by the severity of neurological diseases associated with its disruption [3][4][5] . Given the impact of myelin on neuronal and network physiology, the question of differential regulation of myelination among the many diverse neuron classes in the central nervous system (CNS) is of fundamental importance.…”

Section: Main Textmentioning

confidence: 99%

“…Since tdTomato and eGFP were used to label neurons and oligodendrocytes, respectively, the two fluorophores were simultaneously excited with a Mai Tai HP Ti:Sapphire laser (Spectra-Physics) set at 975 nm (CPN experiments) or 990 nm (PV-IN experiments) and pumped by a 14 W solid state laser delivering 100 fs pulses at a rate of 80 MHz. A 200x200x300 µm 3 (CPN) or 200x200x200 µm3…”

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confidence: 99%

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Neuron-class specific responses govern adaptive remodeling of myelination in the neocortex

Yang

Michel

Jokhi

et al. 2020

Preprint

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Myelination plasticity plays a critical role in neurological function, including learning and memory. However, it is unknown whether this plasticity is enacted through uniform changes across all neuronal subtypes, or whether myelin dynamics vary between neuronal classes to enable fine-tuning of adaptive circuit responses. We performed in vivo two-photon imaging to investigate the dynamics of myelin sheaths along single axons of both excitatory callosal projection neurons and inhibitory parvalbumin+ interneurons in layer 2/3 of adult mouse visual cortex. We find that both neuron types show dynamic, homeostatic myelin remodeling under normal vision. However, monocular deprivation results in experience-dependent adaptive myelin remodeling only in parvalbumin+ interneurons, but not in callosal projection neurons. Monocular deprivation induces an initial increase in elongation events in myelin segments of parvalbumin+ interneurons, followed by a contraction phase affecting a separate cohort of segments. Sensory experience does not alter the generation rate of new myelinating oligodendrocytes, but can recruit pre-existing oligodendrocytes to generate new myelin sheaths. Parvalbumin+ interneurons also show a concomitant increase in axonal branch tip dynamics independent from myelination events. These findings suggest that adaptive myelination is part of a coordinated suite of circuit reconfiguration processes, and demonstrate that distinct classes of neocortical neurons individualize adaptive remodeling of their myelination profiles to diversify circuit tuning in response to sensory experience.

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Section: Main Textmentioning

confidence: 99%

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confidence: 99%

Neuron-class specific responses govern adaptive remodeling of myelination in the neocortex

Yang

Michel

Jokhi

et al. 2020

Preprint

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“…An important aspect of this plasticity is thought to involve de‐novo myelination of relevant axonal networks (Kaller, Lazari, Blanco‐Duque, Sampaio‐Baptista, & Johansen‐Berg, ). In contrast to the PNS, in the CNS, an OL progenitor population (OPCs) is maintained throughout life that responds to a need for new myelination during adulthood (Birey, Kokkosis, & Aguirre, ). OPCs are a continually slowly‐proliferating progenitor population dispersed throughout the CNS, that produce new OLs in response to a need for de‐novo myelination that appears to be required for aspects of learning or as a result of demyelinating pathologies such as multiple sclerosis (Kaller et al, ; McKenzie et al, ; Saab & Nave, ; Xiao et al, ).…”

Section: Peripheral Nerve Homeostasismentioning

confidence: 99%

Schwann cell plasticity‐roles in tissue homeostasis, regeneration, and disease

Stierli

Imperatore

Lloyd

2019

Glia

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How tissues are maintained over a lifetime and repaired following injury are fundamental questions in biology with a disruption to these processes underlying pathologies such as cancer and degenerative disorders. It is becoming increasingly clear that each tissue has a distinct mechanism to maintain homeostasis and respond to injury utilizing different types of stem/progenitor cell populations depending on the insult and/or with a contribution from more differentiated cells that are able to dedifferentiate to aid tissue regeneration. Peripheral nerves are highly quiescent yet show remarkable regenerative capabilities. Remarkably, there is no evidence for a classical stem cell population, rather all cell‐types within the nerve are able to proliferate to produce new nerve tissue. Co‐ordinating the regeneration of this tissue are Schwann cells (SCs), the main glial cells of the peripheral nervous system. SCs exist in architecturally stable structures that can persist for the lifetime of an animal, however, they are not postmitotic, in that following injury they are reprogrammed at high efficiency to a progenitor‐like state, with these cells acting to orchestrate the nerve regeneration process. During nerve regeneration, SCs show little plasticity, maintaining their identity in the repaired tissue. However, once free of the nerve environment they appear to exhibit increased plasticity with reported roles in the repair of other tissues. In this review, we will discuss the mechanisms underlying the homeostasis and regeneration of peripheral nerves and how reprogrammed progenitor‐like SCs have broader roles in the repair of other tissues with implications for pathologies such as cancer.

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“…Indeed, the term oligodendrogliopathy was initially coined by Lassman et al in the context of myein-associated glycoprotein deficiency (Lassmann et al, 1997), and astro-and oligodendrogliopathy are early events in CNS demyelination (Zhang et al, 2013;Rone et al, 2016). Yet disturbances of oligodendrocyte function have also emerged as determining factors in apparently distant diseases such as psychiatric disorders including schizophrenia and major depression (Miyata et al, 2015;Birey et al, 2017).…”

Section: Oligodendrogliopathymentioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

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Oligodendrocytes are in contact with neurons, wrap axons with a myelin sheath that protects their structural integrity, and facilitate nerve conduction. Oligodendrocytes also form a syncytium with astrocytes which interacts with neurons, promoting reciprocal survival mediated by activity and by molecules involved in energy metabolism and trophism. Therefore, oligodendrocytes are key elements in the normal functioning of the central nervous system. Oligodendrocytes are affected following different insults to the central nervous system including ischemia, traumatism, and inflammation. The term oligodendrogliopathy highlights the prominent role of altered oligodendrocytes in the pathogenesis of certain neurological diseases, not only in demyelinating diseases and most leukodystrophies, but also in aging and age-related neurodegenerative diseases with abnormal protein aggregates. Most of these diseases are characterized by the presence of abnormal protein deposits, forming characteristic and specific inclusions in neurons and astrocytes but also in oligodendrocytes, thus signaling their involvement in the disease. Emerging evidence suggests that such deposits in oligodendrocytes are not mere bystanders but rather are associated with functional alterations. Moreover, operative modifications in oligodendrocytes are also detected in the absence of oligodendroglial inclusions in certain diseases. The present review focuses first on general aspects of oligodendrocytes and precursors, and their development and functions, and then introduces and updates alterations and dysfunction of oligodendrocytes in selected neurodegenerative diseases with abnormal protein aggregates such as multiple system atrophy, Lewy body diseases, tauopathies, Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal lobar degeneration with TDP-43 inclusions (TDP-43 proteinopathies), and Creutzfeldt-Jakob´s disease as a prototypical human prionopathy.

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Oligodendroglia-lineage cells in brain plasticity, homeostasis and psychiatric disorders

Cited by 40 publications

References 133 publications

Neuron-class specific responses govern adaptive remodeling of myelination in the neocortex

Neuron-class specific responses govern adaptive remodeling of myelination in the neocortex

Schwann cell plasticity‐roles in tissue homeostasis, regeneration, and disease

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

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