Activity-dependent regulation of myelin maintenance in the adult rat

Canu, Marie‐Hélène; Carnaud, Michèle; Picquet, Florence; Goutebroze, Laurence

doi:10.1016/j.brainres.2008.10.079

Cited by 31 publications

(29 citation statements)

References 28 publications

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“…Physical activity is known to affect conduction velocity, as conditions of inactivity, such as during bed rest or outer space missions, temporarily reduce conduction velocities 56 . Increasing motor activity in rats is associated with altered myelin thickness and axon diameter in peripheral nerves 57 . The results suggest that activity not only influences the formation of myelin, but also influences the maintenance and morphology of the sheath after myelination is complete.…”

Section: Candidate Mechanisms For White Matter Changesmentioning

confidence: 98%

Plasticity in gray and white: neuroimaging changes in brain structure during learning

2012

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Human brain imaging has identified structural changes in gray and white matter that occur with learning. However, ascribing imaging measures to underlying cellular and molecular events is challenging. Here, we review human neuroimaging findings of structural plasticity and then discuss cellular and molecular level changes that could underlie observed imaging effects. We propose that greater dialogue between researchers in these different fields will help to facilitate cross talk between cellular and systems level explanations of how learning sculpts brain structure.

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Section: Candidate Mechanisms For White Matter Changesmentioning

confidence: 98%

Plasticity in gray and white: neuroimaging changes in brain structure during learning

2012

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“…Neuronal activity is also thought to determine the maintenance of the myelin sheath in adult axons. In the hindlimb unloading model, myelin thickness is tightly controlled by motor activity (93). Myelin is thinner in axons controlling inactive muscles but thicker in hyperactive axons.…”

Section: A Morphological Plasticitymentioning

confidence: 99%

Axon Physiology

Debanne

Campanac

Bialowas

et al. 2011

Physiological Reviews

544

492

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Axons are generally considered as reliable transmission cables in which stable propagation occurs once an action potential is generated. Axon dysfunction occupies a central position in many inherited and acquired neurological disorders that affect both peripheral and central neurons. Recent findings suggest that the functional and computational repertoire of the axon is much richer than traditionally thought. Beyond classical axonal propagation, intrinsic voltage-gated ionic currents together with the geometrical properties of the axon determine several complex operations that not only control signal processing in brain circuits but also neuronal timing and synaptic efficacy. Recent evidence for the implication of these forms of axonal computation in the short-term dynamics of neuronal communication is discussed. Finally, we review how neuronal activity regulates both axon morphology and axonal function on a long-term time scale during development and adulthood.

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“…Plasticity of myelination can be revealed when changes in axonal activity are imposed or fiber tracts are lesioned. For example, imposed hind limb load changes induce changes in myelin thickness and internodal length in different peripheral nerves, partly associated with changes in conduction velocity (Canu et al , 2009). Axonal sprouting observed in the hippocampus following lesion of the entorhino-hippocampal perforant pathway is associated with the recruitment of newly formed myelinating cells, suggesting that myelination is still plastic in adult animals (Drojdahl et al , 2010).…”

Section: Long-term Regulation Of Axonal Propertiesmentioning

confidence: 99%

Beyond faithful conduction: Short-term dynamics, neuromodulation, and long-term regulation of spike propagation in the axon

Bucher¹,

Goaillard²

2011

Progress in Neurobiology

170

190

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Most spiking neurons are divided into functional compartments: a dendritic input region, a soma, a site of action potential initiation, an axon trunk and its collaterals for propagation of action potentials, and distal arborizations and terminals carrying the output synapses. The axon trunk and lower order branches are probably the most neglected and are often assumed to do nothing more than faithfully conducting action potentials. Nevertheless, there are numerous reports of complex membrane properties in non-synaptic axonal regions, owing to the presence of a multitude of different ion channels. Many different types of sodium and potassium channels have been described in axons, as well as calcium transients and hyperpolarization-activated inward currents. The complex time- and voltage-dependence resulting from the properties of ion channels can lead to activity-dependent changes in spike shape and resting potential, affecting the temporal fidelity of spike conduction. Neural coding can be altered by activity-dependent changes in conduction velocity, spike failures, and ectopic spike initiation. This is true under normal physiological conditions, and relevant for a number of neuropathies that lead to abnormal excitability. In addition, a growing number of studies show that the axon trunk can express receptors to glutamate, GABA, acetylcholine or biogenic amines, changing the relative contribution of some channels to axonal excitability and therefore rendering the contribution of this compartment to neural coding conditional on the presence of neuromodulators. Long-term regulatory processes, both during development and in the context of activity-dependent plasticity may also affect axonal properties to an underappreciated extent.

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Activity-dependent regulation of myelin maintenance in the adult rat

Cited by 31 publications

References 28 publications

Plasticity in gray and white: neuroimaging changes in brain structure during learning

Plasticity in gray and white: neuroimaging changes in brain structure during learning

Axon Physiology

Beyond faithful conduction: Short-term dynamics, neuromodulation, and long-term regulation of spike propagation in the axon

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