• Je něco špatně v tomto záznamu ?

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

. 2013 ; 62 (1) : 95-105.

Jazyk angličtina Země Česko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc13033366

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.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc13033366
003      
CZ-PrNML
005      
20131031091958.0
007      
ta
008      
131015s2013 xr da f 000 0|eng||
009      
AR
024    7_
$a 10.33549/physiolres.932264 $2 doi
035    __
$a (PubMed)23173681
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xr
100    1_
$a Zschüntzsch, J. $u Department of Neurology, Georg-August-University, Göttingen, Germany
245    10
$a Heterologous expression of a glial Kir channel (KCNJ10) in a neuroblastoma spinal cord (NSC-34) cell line / $c J. Zschüntzsch, S. Schütze, S. Hülsmann, P. Dibaj, C. Neusch
520    9_
$a 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.
650    _2
$a zvířata $7 D000818
650    _2
$a nádorové buněčné linie $7 D045744
650    _2
$a zelené fluorescenční proteiny $x genetika $x metabolismus $7 D049452
650    _2
$a membránové potenciály $7 D008564
650    _2
$a myši $7 D051379
650    _2
$a napěťově řízený sodíkový kanál, typ 6 $x metabolismus $7 D062557
650    _2
$a neuroblastom $x genetika $x metabolismus $7 D009447
650    _2
$a metoda terčíkového zámku $7 D018408
650    _2
$a draslíkové kanály dovnitř usměrňující $x genetika $x metabolismus $7 D024661
650    _2
$a rekombinantní fúzní proteiny $x metabolismus $7 D011993
650    _2
$a nádory míchy $x genetika $x metabolismus $7 D013120
650    _2
$a transfekce $7 D014162
655    _2
$a časopisecké články $7 D016428
700    1_
$a Schütze, S. $u Department of Neurology, Georg-August-University, Göttingen, Germany
700    1_
$a Hülsmann, S. $u Department of Neurophysiology and Cellular Biophysics, Georg-August-University, Göttingen, Germany
700    1_
$a Dibaj, P. $u Max-Planck-Institute for Experimental Medicine, Göttingen, Germany
700    1_
$a Neusch, C. $u Department of Neurology, Georg-August-University, Göttingen, Germany; Department of Neurology, University of Ulm, Germany
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 62, č. 1 (2013), s. 95-105
856    41
$u http://www.biomed.cas.cz/physiolres/archive.htm $y domovská stránka časopisu - plný text volně přístupný = fulltext
910    __
$a ABA008 $b A 4120 $c 266 $y 3 $z 0
990    __
$a 20131015 $b ABA008
991    __
$a 20131031092409 $b ABA008
999    __
$a ok $b bmc $g 999117 $s 831820
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2013 $b 62 $c 1 $d 95-105 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
LZP    __
$b NLK111 $a Pubmed-20131015

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...