Effects of Axonal Demyelination, Inflammatory Cytokines and Divalent Cation Chelators on Thalamic HCN Channels and Oscillatory Bursting.
brain slice
computational modeling
cuprizone model
expression system
firing pattern
ion channels
patch-clamp
thalamus
trace metal
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
03 Jun 2022
03 Jun 2022
Historique:
received:
27
04
2022
revised:
31
05
2022
accepted:
31
05
2022
entrez:
10
6
2022
pubmed:
11
6
2022
medline:
14
6
2022
Statut:
epublish
Résumé
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system that is characterized by the progressive loss of oligodendrocytes and myelin and is associated with thalamic dysfunction. Cuprizone (CPZ)-induced general demyelination in rodents is a valuable model for studying different aspects of MS pathology. CPZ feeding is associated with the altered distribution and expression of different ion channels along neuronal somata and axons. However, it is largely unknown whether the copper chelator CPZ directly influences ion channels. Therefore, we assessed the effects of different divalent cations (copper; zinc) and trace metal chelators (EDTA; Tricine; the water-soluble derivative of CPZ, BiMPi) on hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that are major mediators of thalamic function and pathology. In addition, alterations of HCN channels induced by CPZ treatment and MS-related proinflammatory cytokines (IL-1β; IL-6; INF-α; INF-β) were characterized in C57Bl/6J mice. Thus, the hyperpolarization-activated inward current (I
Identifiants
pubmed: 35682964
pii: ijms23116285
doi: 10.3390/ijms23116285
pmc: PMC9181513
pii:
doi:
Substances chimiques
Cations, Divalent
0
Chelating Agents
0
Cytokines
0
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
0
Copper
789U1901C5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : GRK 2515
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB-TRR 128/B06
Organisme : Deutsche Forschungsgemeinschaft
ID : BU 1019/16-1
Organisme : Deutsche Forschungsgemeinschaft
ID : SE 1077/13-1
Organisme : Federal Institute for Risk Assessment
ID : 60-0102-01.P585
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