Wrapped to Adapt: Experience-Dependent Myelination

Mount, Christopher; Monje, Michelle

doi:10.1016/j.neuron.2017.07.009

Cited by 201 publications

(190 citation statements)

References 153 publications

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“…Internodes were measured across n = 3 mice per treatment group [Color figure can be viewed at wileyonlinelibrary.com] iTBS produced this effect without influencing oligodendrogenesis (OPC proliferation or differentiation; Figure 3). This outcome was unexpected, as both 10 Hz and iTBS are predicted to increase neuronal activity, which is a potent modulator of OPC proliferation and differentiation within the CNS (reviewed by Mount & Monje, 2017). For example, a 5 Hz stimulation of the CC in freely behaving mice (single 3 hr session via implanted electrodes), can promote OPC differentiation without significantly increasing proliferation (Nagy, Hovhannisyan, Barzan, Chen, & Kukley, 2017).…”

Section: Itbs Does Not Increase Oligodendrogenesismentioning

confidence: 99%

Low‐intensity transcranial magnetic stimulation promotes the survival and maturation of newborn oligodendrocytes in the adult mouse brain

Cullen

Senesi

Tang

et al. 2019

Glia

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Neuronal activity is a potent extrinsic regulator of oligodendrocyte generation and central nervous system myelination. Clinically, repetitive transcranial magnetic stimulation (rTMS) is delivered to noninvasively modulate neuronal activity; however, the ability of rTMS to facilitate adaptive myelination has not been explored. By performing cre‐lox lineage tracing, to follow the fate of oligodendrocyte progenitor cells in the adult mouse brain, we determined that low intensity rTMS (LI‐rTMS), administered as an intermittent theta burst stimulation, but not as a continuous theta burst or 10 Hz stimulation, increased the number of newborn oligodendrocytes in the adult mouse cortex. LI‐rTMS did not alter oligodendrogenesis per se, but instead increased cell survival and enhanced myelination. These data suggest that LI‐rTMS can be used to noninvasively promote myelin addition to the brain, which has potential implications for the treatment of demyelinating diseases such as multiple sclerosis.

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Section: Itbs Does Not Increase Oligodendrogenesismentioning

confidence: 99%

Low‐intensity transcranial magnetic stimulation promotes the survival and maturation of newborn oligodendrocytes in the adult mouse brain

Cullen

Senesi

Tang

et al. 2019

Glia

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“…Such developmental delay may enhance the impact of postnatal experience on myelination. Indeed, there is now considerable amount of data providing evidence that myelination is not fully determined by intrinsic genetic programs, but also subject to modification by environmental factors (Fields, ; Forbes & Gallo, ; Mount & Monje, ). Here, we will summarize our current understanding of grey matter myelination including its emerging role in shaping neuronal cortical circuits.…”

Section: Introductionmentioning

confidence: 99%

Grey matter myelination

Timmler

Simons

2019

Glia

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There is now increasing evidence that myelin is not only generated early in development, but also during adulthood possibly contributing to lifelong plasticity of the brain. In particular, human cortical areas responsible for the highest cognitive functions seem to require decades until they have reached their maximal amount of myelination. Currently, we know very little about the mechanisms and the functions of grey matter myelination. In this emerging field key questions await to be addressed: How long does myelination last in humans? How is grey matter myelination regulated? What is the function of myelin in the grey matter? Does grey matter myelination limit and/or promote neuronal plasticity? Finding answers to these questions will be important for our understanding of normal, but also abnormal cortex function in a number of neurological and psychiatric diseases.

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“…It is however remarkable that the patient with GLS hyperactivity and glutamate excess in the brain did not develop seizures. Glutamate induces myelination of axons and it is therefore not surprising that white matter and myelin abnormalities are frequently reported in patients with an inborn error of glutamate metabolism . Although this is an a‐specific sign seen in many disorders, it is more prevalent in glutamate related disorders than in all Mendelian disorders (14‐16×) and in all disorders with metabolic abnormalities (9‐13×).…”

Section: Discussionmentioning

confidence: 99%

“…Glutamate induces myelination of axons and it is therefore not surprising that white matter and myelin abnormalities are frequently reported in patients with an inborn error of glutamate metabolism. 2 Although this is an a-specific sign seen in many disorders, it is more prevalent in glutamate related disorders than in all Mendelian disorders (14-16×) and in all disorders with metabolic abnormalities (9-13×). Patients with inborn errors of glutamate metabolism caused by defects of glutamate receptors and transporters also present with neurological disorders, like seizures, ataxia and developmental delay, underlying the clinical importance of balanced glutamate metabolism for the human brain.…”

Section: Discussionmentioning

confidence: 99%

“…The amino acids glutamate and glutamine are key players in metabolism, functioning as both substrate and product in various enzymatic reactions . Glutamate is the main excitatory neurotransmitter in the central nervous system and triggers responses implicated in neuronal migration and differentiation, synapse remodelling and axon myelination . Additionally, glutamate is the precursor of glutathione and the tricarboxylic acid (TCA) cycle intermediates and therefore plays a role in redox state and energy metabolism respectively .…”

Section: Introductionmentioning

confidence: 99%

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Inborn errors of enzymes in glutamate metabolism

Rumping

Vringer

Houwen

et al. 2019

J of Inher Metab Disea

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Glutamate is involved in a variety of metabolic pathways. We reviewed the literature on genetic defects of enzymes that directly metabolise glutamate, leading to inborn errors of glutamate metabolism. Seventeen genetic defects of glutamate metabolising enzymes have been reported, of which three were only recently identified. These 17 defects affect the inter‐conversion of glutamine and glutamate, amino acid metabolism, ammonia detoxification, and glutathione metabolism. We provide an overview of the clinical and biochemical phenotypes of these rare defects in an effort to ease their recognition. By categorising these by biochemical pathway, we aim to create insight into the contributing role of deviant glutamate and glutamine levels to the pathophysiology. For those disorders involving the inter‐conversion of glutamine and glutamate, these deviant levels are postulated to play a pivotal pathophysiologic role. For the other IEM however—with the exception of urea cycle defects—abnormal glutamate and glutamine concentrations were rarely reported. To create insight into the clinical consequences of disturbed glutamate metabolism—rather than individual glutamate and glutamine levels—the prevalence of phenotypic abnormalities within the 17 IEM was compared to their prevalence within all Mendelian disorders and subsequently all disorders with metabolic abnormalities notated in the Human Phenotype Ontology (HPO) database. For this, a hierarchical database of all phenotypic abnormalities of the 17 defects in glutamate metabolism based on HPO was created. A neurologic phenotypic spectrum of developmental delay, ataxia, seizures, and hypotonia are common in the inborn errors of enzymes in glutamate metabolism. Additionally, ophthalmologic and skin abnormalities are often present, suggesting that disturbed glutamate homeostasis affects tissues of ectodermal origin: brain, eye, and skin. Reporting glutamate and glutamine concentrations in patients with inborn errors of glutamate metabolism would provide additional insight into the pathophysiology.

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