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Neurotransmitter receptors in the life and death of oligodendrocytes

Oligodendrocytes are crucial to the function of the mammalian brain: they increase the action potential conduction speed for a given axon diameter and thus facilitate the rapid flow of information between different brain areas. The proliferation and differentiation of developing oligodendrocytes, an...

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Detalles Bibliográficos
Autores principales: Káradóttir, R., Attwell, D.
Formato: Texto
Lenguaje:English
Publicado: Elsevier Science 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2173944/
https://www.ncbi.nlm.nih.gov/pubmed/17049173
http://dx.doi.org/10.1016/j.neuroscience.2006.08.070
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author Káradóttir, R.
Attwell, D.
author_facet Káradóttir, R.
Attwell, D.
author_sort Káradóttir, R.
collection PubMed
description Oligodendrocytes are crucial to the function of the mammalian brain: they increase the action potential conduction speed for a given axon diameter and thus facilitate the rapid flow of information between different brain areas. The proliferation and differentiation of developing oligodendrocytes, and their myelination of axons, are partly controlled by neurotransmitters. In addition, in models of conditions like stroke, periventricular leukomalacia leading to cerebral palsy, spinal cord injury and multiple sclerosis, oligodendrocytes are damaged by glutamate and, contrary to dogma, it has recently been discovered that this damage is mediated in part by N-methyl-d-aspartate receptors. Mutations in oligodendrocyte neurotransmitter receptors or their interacting proteins may cause defects in CNS function. Here we review the roles of neurotransmitter receptors in the normal function, and malfunction in pathological conditions, of oligodendrocytes.
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spelling pubmed-21739442008-01-03 Neurotransmitter receptors in the life and death of oligodendrocytes Káradóttir, R. Attwell, D. Neuroscience Excitotoxicity, oxidative stress and DNA damage in relation to amino acid neurotransmission Oligodendrocytes are crucial to the function of the mammalian brain: they increase the action potential conduction speed for a given axon diameter and thus facilitate the rapid flow of information between different brain areas. The proliferation and differentiation of developing oligodendrocytes, and their myelination of axons, are partly controlled by neurotransmitters. In addition, in models of conditions like stroke, periventricular leukomalacia leading to cerebral palsy, spinal cord injury and multiple sclerosis, oligodendrocytes are damaged by glutamate and, contrary to dogma, it has recently been discovered that this damage is mediated in part by N-methyl-d-aspartate receptors. Mutations in oligodendrocyte neurotransmitter receptors or their interacting proteins may cause defects in CNS function. Here we review the roles of neurotransmitter receptors in the normal function, and malfunction in pathological conditions, of oligodendrocytes. Elsevier Science 2007-04-14 /pmc/articles/PMC2173944/ /pubmed/17049173 http://dx.doi.org/10.1016/j.neuroscience.2006.08.070 Text en © 2007 Elsevier Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license
spellingShingle Excitotoxicity, oxidative stress and DNA damage in relation to amino acid neurotransmission
Káradóttir, R.
Attwell, D.
Neurotransmitter receptors in the life and death of oligodendrocytes
title Neurotransmitter receptors in the life and death of oligodendrocytes
title_full Neurotransmitter receptors in the life and death of oligodendrocytes
title_fullStr Neurotransmitter receptors in the life and death of oligodendrocytes
title_full_unstemmed Neurotransmitter receptors in the life and death of oligodendrocytes
title_short Neurotransmitter receptors in the life and death of oligodendrocytes
title_sort neurotransmitter receptors in the life and death of oligodendrocytes
topic Excitotoxicity, oxidative stress and DNA damage in relation to amino acid neurotransmission
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2173944/
https://www.ncbi.nlm.nih.gov/pubmed/17049173
http://dx.doi.org/10.1016/j.neuroscience.2006.08.070
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