Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]

Oligodendrocytes wrap multiple lamellae of their membrane, myelin, around axons of the central nervous system (CNS), to improve impulse conduction. Myelin synthesis is specialised and dynamic, responsive to local neuronal excitation. Subtle pathological insults are sufficient to cause significant ne...

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Autores principales:	Maddalena Rupnik, David Baker, David L. Selwood
Formato:	article
Lenguaje:	EN
Publicado:	F1000 Research Ltd 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9810d00c370c4920b32bff4a8c35f151
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spelling	oai:doaj.org-article:9810d00c370c4920b32bff4a8c35f1512021-11-22T12:41:06ZOligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]2046-140210.12688/f1000research.53422.2https://doaj.org/article/9810d00c370c4920b32bff4a8c35f1512021-11-01T00:00:00Zhttps://f1000research.com/articles/10-781/v2https://doaj.org/toc/2046-1402Oligodendrocytes wrap multiple lamellae of their membrane, myelin, around axons of the central nervous system (CNS), to improve impulse conduction. Myelin synthesis is specialised and dynamic, responsive to local neuronal excitation. Subtle pathological insults are sufficient to cause significant neuronal metabolic impairment, so myelin preservation is necessary to safeguard neural networks. Multiple sclerosis (MS) is the most prevalent demyelinating disease of the CNS. In MS, inflammatory attacks against myelin, proposed to be autoimmune, cause myelin decay and oligodendrocyte loss, leaving neurons vulnerable. Current therapies target the prominent neuroinflammation but are mostly ineffective in protecting from neurodegeneration and the progressive neurological disability. People with MS have substantially higher levels of extracellular glutamate, the main excitatory neurotransmitter. This impairs cellular homeostasis to cause excitotoxic stress. Large conductance Ca2+-activated K+ channels (BK channels) could preserve myelin or allow its recovery by protecting cells from the resulting excessive excitability. This review evaluates the role of excitotoxic stress, myelination and BK channels in MS pathology, and explores the hypothesis that BK channel activation could be a therapeutic strategy to protect oligodendrocytes from excitotoxic stress in MS. This could reduce progression of neurological disability if used in parallel to immunomodulatory therapies.Maddalena RupnikDavid BakerDavid L. SelwoodF1000 Research LtdarticleMedicineRScienceQENF1000Research, Vol 10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Maddalena Rupnik David Baker David L. Selwood Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
description	Oligodendrocytes wrap multiple lamellae of their membrane, myelin, around axons of the central nervous system (CNS), to improve impulse conduction. Myelin synthesis is specialised and dynamic, responsive to local neuronal excitation. Subtle pathological insults are sufficient to cause significant neuronal metabolic impairment, so myelin preservation is necessary to safeguard neural networks. Multiple sclerosis (MS) is the most prevalent demyelinating disease of the CNS. In MS, inflammatory attacks against myelin, proposed to be autoimmune, cause myelin decay and oligodendrocyte loss, leaving neurons vulnerable. Current therapies target the prominent neuroinflammation but are mostly ineffective in protecting from neurodegeneration and the progressive neurological disability. People with MS have substantially higher levels of extracellular glutamate, the main excitatory neurotransmitter. This impairs cellular homeostasis to cause excitotoxic stress. Large conductance Ca2+-activated K+ channels (BK channels) could preserve myelin or allow its recovery by protecting cells from the resulting excessive excitability. This review evaluates the role of excitotoxic stress, myelination and BK channels in MS pathology, and explores the hypothesis that BK channel activation could be a therapeutic strategy to protect oligodendrocytes from excitotoxic stress in MS. This could reduce progression of neurological disability if used in parallel to immunomodulatory therapies.
format	article
author	Maddalena Rupnik David Baker David L. Selwood
author_facet	Maddalena Rupnik David Baker David L. Selwood
author_sort	Maddalena Rupnik
title	Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
title_short	Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
title_full	Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
title_fullStr	Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
title_full_unstemmed	Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]
title_sort	oligodendrocytes, bk channels and the preservation of myelin [version 2; peer review: 2 approved]
publisher	F1000 Research Ltd
publishDate	2021
url	https://doaj.org/article/9810d00c370c4920b32bff4a8c35f151
work_keys_str_mv	AT maddalenarupnik oligodendrocytesbkchannelsandthepreservationofmyelinversion2peerreview2approved AT davidbaker oligodendrocytesbkchannelsandthepreservationofmyelinversion2peerreview2approved AT davidlselwood oligodendrocytesbkchannelsandthepreservationofmyelinversion2peerreview2approved
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Oligodendrocytes, BK channels and the preservation of myelin [version 2; peer review: 2 approved]

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