RGD Reference Report - Impact of global cerebral ischemia on K+ channel expression and membrane properties of glial cells in the rat hippocampus. - Rat Genome Database

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Impact of global cerebral ischemia on K+ channel expression and membrane properties of glial cells in the rat hippocampus.

Authors: Pivonkova, H  Benesova, J  Butenko, O  Chvatal, A  Anderova, M 
Citation: Pivonkova H, etal., Neurochem Int. 2010 Dec;57(7):783-94. doi: 10.1016/j.neuint.2010.08.016. Epub 2010 Sep 15.
RGD ID: 8662899
Pubmed: (View Article at PubMed) PMID:20833221
DOI: Full-text: DOI:10.1016/j.neuint.2010.08.016

Astrocytes and NG2 glia respond to CNS injury by the formation of a glial scar. Since the changes in K(+) currents in astrocytes and NG2 glia that accompany glial scar formation might influence tissue outcome by altering K(+) ion homeostasis, we aimed to characterize the changes in K(+) currents in hippocampal astrocytes and NG2 glia during an extended time window of reperfusion after ischemic injury. Global cerebral ischemia was induced in adult rats by bilateral, 15-min common carotid artery occlusion combined with low-pressure oxygen ventilation. Using the patch-clamp technique, we investigated the membrane properties of hippocampal astrocytes and NG2 glia in situ 2 hours, 6 hours, 1 day, 3 days, 7 days or 5 weeks after ischemia. Astrocytes in the CA1 region of the hippocampus progressively depolarized starting 3 days after ischemia, which coincided with decreased Kir4.1 protein expression in the gliotic tissue. Other K(+) channels described previously in astrocytes, such as Kir2.1, Kir5.1 and TREK1, did not show any changes in their protein content in the hippocampus after ischemia; however, their expression switched from neurons to reactive astrocytes, as visualized by immunohistochemistry. NG2 glia displayed increased input resistance, decreased membrane capacitance, increased delayed outwardly rectifying and A-type K(+) currents and decreased inward K(+) currents 3 days after ischemia, accompanied by their proliferation. Our results show that the membrane properties of astrocytes after ischemia undergo complex alterations, which might profoundly influence the maintenance of K(+) homeostasis in the damaged tissue, while NG2 glia display membrane currents typical of proliferating cells.



Disease Annotations    

Gene Ontology Annotations    

Cellular Component

Objects Annotated

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

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

Genes (Homo sapiens)
KCNJ10  (potassium inwardly rectifying channel subfamily J member 10)


Additional Information