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Heterologous expression of a glial Kir channel (KCNJ10) in a neuroblastoma spinal cord (NSC-34) cell line
J. Zschüntzsch, S. Schütze, S. Hülsmann, P. Dibaj, C. Neusch
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- draslíkové kanály dovnitř usměrňující genetika metabolismus MeSH
- membránové potenciály MeSH
- metoda terčíkového zámku MeSH
- myši MeSH
- nádorové buněčné linie MeSH
- nádory míchy genetika metabolismus MeSH
- napěťově řízený sodíkový kanál, typ 6 metabolismus MeSH
- neuroblastom genetika metabolismus MeSH
- rekombinantní fúzní proteiny metabolismus MeSH
- transfekce MeSH
- zelené fluorescenční proteiny genetika metabolismus MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Heterologous expression of Kir channels offers a tool to modulate excitability of neurons which provide insight into Kir channel functions in general. Inwardly-rectifying K+ channels (Kir channels) are potential candidate proteins to hyperpolarize neuronal cell membranes. However, heterologous expression of inwardly-rectifying K+ channels has previously proven to be difficult. This was mainly due to a high toxicity of the respective Kir channel expression. We investigated the putative role of a predominantly glial-expressed, weakly rectifying Kir channel (Kir4.1 channel subunit; KCNJ10) in modulating electrophysiological properties of a motoneuron-like cell culture (NSC-34). Transfection procedures using an EGFP-tagged Kir4.1 protein in this study proved to have no toxic effects on NSC-34 cells. Using whole cell-voltage clamp, a substantial increase of inward rectifying K+ currents as well as hyperpolarization of the cell membrane was observed in Kir4.1-transfected cells. Na+ inward currents, observed in NSC-34 controls, were absent in Kir4.1/EGFP motoneuronal cells. The Kir4.1-transfection did not influence the NaV1.6 sodium channel expression. This study demonstrates the general feasibility of a heterologous expression of a weakly inward-rectifying K+ channel (Kir4.1 subunit) and shows that in vitro overexpression of Kir4.1 shifts electrophysiological properties of neuronal cells to a more glial-like phenotype and may therefore be a candidate tool to dampen excitability of neurons in experimental paradigms.
Department of Neurology Georg August University Göttingen Germany
Department of Neurology University of Ulm Germany
Department of Neurophysiology and Cellular Biophysics Georg August University Göttingen Germany
Max Planck Institute for Experimental Medicine Göttingen Germany
Citace poskytuje Crossref.org
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