Impact of global cerebral ischemia on K+ channel expression and membrane properties of glial cells in the rat hippocampus
Language English Country England, Great Britain Media print-electronic
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
PubMed
20833221
DOI
10.1016/j.neuint.2010.08.016
PII: S0197-0186(10)00271-8
Knihovny.cz E-resources
- MeSH
- Cell Membrane metabolism pathology MeSH
- Down-Regulation genetics physiology MeSH
- Potassium Channels, Inwardly Rectifying antagonists & inhibitors biosynthesis genetics MeSH
- Gliosis genetics metabolism pathology MeSH
- CA1 Region, Hippocampal metabolism pathology physiopathology MeSH
- Brain Ischemia metabolism pathology physiopathology MeSH
- Rats MeSH
- Membrane Potentials physiology MeSH
- Neuroglia metabolism pathology MeSH
- Cell Polarity physiology MeSH
- Rats, Wistar MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- Potassium Channels, Inwardly Rectifying MeSH
- Kcnj10 Channel MeSH
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.
References provided by Crossref.org
Transient astrocyte-like NG2 glia subpopulation emerges solely following permanent brain ischemia
Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells
Altered astrocytic swelling in the cortex of α-syntrophin-negative GFAP/EGFP mice
Polydendrocytes display large lineage plasticity following focal cerebral ischemia