RGD Reference Report - Downregulation of Kir4.1 inward rectifying potassium channel subunits by RNAi impairs potassium transfer and glutamate uptake by cultured cortical astrocytes. - Rat Genome Database

RGD Reference Report - Downregulation of Kir4.1 inward rectifying potassium channel subunits by RNAi impairs potassium transfer and glutamate uptake by cultured cortical astrocytes. - Rat Genome Database

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Downregulation of Kir4.1 inward rectifying potassium channel subunits by RNAi impairs potassium transfer and glutamate uptake by cultured cortical astrocytes.
Authors:	Kucheryavykh, YV Kucheryavykh, LY Nichols, CG Maldonado, HM Baksi, K Reichenbach, A Skatchkov, SN Eaton, MJ
Citation:	Kucheryavykh YV, etal., Glia. 2007 Feb;55(3):274-81.
RGD ID:	2326042
Pubmed:	PMID:17091490 (View Abstract at PubMed)
DOI:	DOI:10.1002/glia.20455 (Journal Full-text)
Glial cell-mediated potassium and glutamate homeostases play important roles in the regulation of neuronal excitability. Diminished potassium and glutamate buffering capabilities of astrocytes result in hyperexcitability of neurons and abnormal synaptic transmission. The role of the different K+ channels in maintaining the membrane potential and buffering capabilities of cortical astrocytes has not yet been definitively determined due to the lack of specific K+ channel blockers. The purpose of the present study was to assess the role of the inward-rectifying K+ channel subunit Kir4.1 on potassium fluxes, glutamate uptake and membrane potential in cultured rat cortical astrocytes using RNAi, whole-cell patch clamp and a colorimetric assay. The membrane potentials of control cortical astrocytes had a bimodal distribution with peaks at -68 and -41 mV. This distribution became unimodal after knockdown of Kir4.1, with the mean membrane potential being shifted in the depolarizing direction (peak at -45 mV). The ability of Kir4.1-suppressed cells to mediate transmembrane potassium flow, as measured by the current response to voltage ramps or sequential application of different extracellular [K+], was dramatically impaired. In addition, glutamate uptake was inhibited by knock-down of Kir4.1-containing channels by RNA interference as well as by blockade of Kir channels with barium (100 microM). Together, these data indicate that Kir4.1 channels are primarily responsible for significant hyperpolarization of cortical astrocytes and are likely to play a major role in potassium buffering. Significant inhibition of glutamate clearance in astrocytes with knock-down of Kir4.1 highlights the role of membrane hyperpolarization in this process.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Kcnj10	Rat	L-glutamate import		IMP			RGD
Kcnj10	Rat	membrane hyperpolarization		IMP			RGD
Kcnj10	Rat	potassium ion import across plasma membrane		IMP			RGD

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Genes (Rattus norvegicus)

Kcnj10 (potassium inwardly-rectifying channel, subfamily J, member 10)

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