title: Impact of global cerebral ischemia on K+ channel expression and membrane properties of glial cells in the rat hippocampus.
abstract: 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.
authors.affiliation: Department of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
authors.forename: Helena
authors.initials: H
authors.lastname: Pivonkova
authors.forename: Jana
authors.initials: J
authors.lastname: Benesova
authors.forename: Olena
authors.initials: O
authors.lastname: Butenko
authors.forename: Alexandr
authors.initials: A
authors.lastname: Chvatal
authors.forename: Miroslava
authors.initials: M
authors.lastname: Anderova
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D056547:CA1 Region, Hippocampal / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002462:Cell Membrane / Q000378:metabolism* / Q000473:pathology; D016764:Cell Polarity / Q000502:physiology*; D015536:Down-Regulation / Q000235:genetics / Q000502:physiology; D005911:Gliosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008564:Membrane Potentials / Q000502:physiology*; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D024661:Potassium Channels, Inwardly Rectifying / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D000098854:Kcnj10 Channel
chemical_list: D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying