Cuprizone feeding induces swollen astrocyte endfeet.

Aquaporin-4 Astrocytic endfeet Cuprizone Edema Electron microscopy Multiple sclerosis Orthogonal arrays of particles (OAPs)

Journal

Pflugers Archiv : European journal of physiology
ISSN: 1432-2013
Titre abrégé: Pflugers Arch
Pays: Germany
ID NLM: 0154720

Informations de publication

Date de publication:
12 2022
Historique:
received: 11 04 2022
accepted: 04 10 2022
revised: 29 09 2022
pubmed: 15 10 2022
medline: 18 11 2022
entrez: 14 10 2022
Statut: ppublish

Résumé

The cuprizone model is a widely used model to study the pathogenesis of multiple sclerosis (MS). Due to the selective loss of mature oligodendrocytes and myelin, it is mainly being used to study demyelination and the mechanisms of remyelination, as well as the efficiency of compounds or therapeutics aiming at remyelination. Although early investigations using high dosages of cuprizone reported the occurrence of hydrocephalus, it has long been assumed that cuprizone feeding at lower dosages does not induce changes at the blood-brain barrier (BBB). Here, by analyzing BBB ultrastructure with high-resolution electron microscopy, we report changes at astrocytic endfeet surrounding vessels in the brain parenchyma. Particularly, edema formation around blood vessels and swollen astrocytic endfeet already occurred after feeding low dosages of cuprizone. These findings indicate changes in BBB function that will have an impact on the milieu of the central nervous system (CNS) in the cuprizone model and need to be considered when studying the mechanisms of de- and remyelination.

Identifiants

pubmed: 36241864
doi: 10.1007/s00424-022-02759-8
pii: 10.1007/s00424-022-02759-8
pmc: PMC9663402
doi:

Substances chimiques

Cuprizone 5N16U7E0AO

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1275-1283

Informations de copyright

© 2022. The Author(s).

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Auteurs

Petra Fallier-Becker (P)

Institute of Pathology and Neuropathology, University Hospital Tübingen, Tübingen, Germany.

Irina Bonzheim (I)

Institute of Pathology and Neuropathology, University Hospital Tübingen, Tübingen, Germany.

Friederike Pfeiffer (F)

Department of Neurophysiology, Institute of Physiology, Eberhard Karls University of Tübingen, Tübingen, Germany. friederike.pfeiffer@uni-tuebingen.de.

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