|  Help  |  About  |  Contact Us

Publication : The contribution of TWIK-1 channels to astrocyte K(+) current is limited by retention in intracellular compartments.

First Author  Wang W Year  2013
Journal  Front Cell Neurosci Volume  7
Pages  246 PubMed ID  24368895
Mgi Jnum  J:244846 Mgi Id  MGI:5913625
Doi  10.3389/fncel.2013.00246 Citation  Wang W, et al. (2013) The contribution of TWIK-1 channels to astrocyte K(+) current is limited by retention in intracellular compartments. Front Cell Neurosci 7:246
abstractText  TWIK-1 two-pore domain K(+) channels are expressed abundantly in astrocytes. In the present study, we examined the extent to which TWIK-1 contributes to the linear current-voltage (I-V) relationship (passive) K(+) membrane conductance, a dominant electrophysiological feature of mature hippocampal astrocytes. Astrocytes from TWIK-1 knockout mice have a more negative resting potential than those from wild type animals and a reduction in both inward rectification and Cs(+) permeability. Nevertheless, the overall whole-cell passive conductance is not altered significantly in TWIK-1 knockout astrocytes. The expression of Kir4.1 and TREK-1, two other major astrocytic K(+) channels, or of other two-pore K(+) channels is not altered in TWIK-1 knockout mice, suggesting that the mild effect of TWIK-1 knockout does not result from compensation by these channels. Fractionation experiments showed that TWIK-1 is primarily localized in intracellular cytoplasmic fractions (55%) and mildly hydrophobic internal compartment fractions (41%), with only 5% in fractions containing plasma membranes. Our study revealed that TWIK-1 proteins are mainly located in the intracellular compartments of hippocampal astrocyte under physiological condition, therefore a minimal contribution of TWIK-1 channels to whole-cell currents is likely attributable to a relatively low level presence of channels in the plasma membrane.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

4 Bio Entities

Trail: Publication

0 Expression