Heterologous expression of a glial kir channel (KCNJ10) in a neuroblastoma spinal cord (NSC-34) cell line

Title:

Heterologous expression of a glial kir channel (KCNJ10) in a neuroblastoma spinal cord (NSC-34) cell line

Creator:

Zschüntzsch, J., Schütze, S., Hülsmann, S., Dibaj, P., and Neusch, C.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:967a7571-e48c-4d1b-be11-fe86361336f9
uuid:967a7571-e48c-4d1b-be11-fe86361336f9

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, kir channels, motoneuron, patch clamp, neuronal excitability, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

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 gliallike phenotype and may therefore be a candidate tool to dampen excitability of neurons in experimental paradigms., J. Zschüntzsch, ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2013 Volume:62 | Number:1

Harvested from:

CDK

Metadata only:

false