Functional implications for Kir4.1 channels in glial biology: from K + buffering to cell differentiation
Open accessAbstract
Astrocytes and oligodendrocytes are characterized by a very negative resting potential and a high resting permeability for K + ions. Early pharmacological and biophysical studies suggested that the resting potential is established by the activity of inwardly rectifying, Ba 2+ sensitive, weakly rectifying Kir channels. Molecular cloning has identified 16 Kir channels genes of which several mRNA transcripts and protein products have been identified in glial cells. However, genetic deletion and siRNA knock‐down studies suggest that the resting conductance of astrocytes and oligodendrocytes is largely due to Kir4.1. Loss of Kir4.1 causes membrane depolarization, and a break‐down of K + and glutamate homeostasis which results in seizures and wide‐spread white matter pathology. Kir channels have also been shown to act as critical regulators of cell division whereby Kir function is correlated with an exit from the cell cycle. Conversely, loss of functional Kir channels is associated with re‐entry of cells into the cell cycle and gliosis. A loss of functional Kir channels has been shown in a number of neurological diseases including temporal lobe epilepsy, amyotrophic lateral sclerosis, retinal degeneration and malignant gliomas. In the latter, expression of Kir4.1 is sufficient to arrest the aberrant growth of these glial derived tumor cells. Kir4.1 therefore represents a potential therapeutic target in a wide variety of neurological conditions.
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TSC2−/− organoids show increased expression of Cx43 and Kir4.1.
“We also observed increased expression of the gap junction protein Cx43 and the potassium channel Kir4.1, which mediate astrocyte intercellular communication and potassium buffering, respectively39,40 (Fig. 3g,h and Extended Data Fig. 7e,f).”
From mTORC1 drives cell-autonomous astrocyte reactivity in tuberous sclerosis (2026) · cites this paper as [40]
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Higashimori, H., & Sontheimer, H. (2007) · Glia · doi:10.1002/glia.20574 · Cited by 101 · see citing works
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- Authors
- Olsen, M. L., & Sontheimer, H.
- Affiliations
- University of Alabama (US)
- University of Alabama at Birmingham (US)
- Corresponding author
- Sontheimer, Harald
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2008-10-14
- Volume
- 107
- Issue
- 3
- Pages
- 589-601
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC2581639
- OpenAlex
- W1981893433
- Cited by
- 323
- References
- 1
- Citations by year
- 2026: 14 · 2025: 22 · 2024: 11 · 2023: 23 · 2022: 16 · 2021: 19 · 2020: 20 · 2019: 22 · 2018: 16 · 2017: 16 · 2016: 23 · 2015: 15 · 2014: 26 · 2013: 20 · 2012: 27
- FWCI
- 0.85
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (5r01ns031234-18, RO1 NS-31234)
- National Institute of Neurological Disorders and Stroke (R01-NS031234, R01-NS--31234, R01NS052634, R01 NS-52634, R01 NS 36692, R01NS036692)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Kir4.1, inwardly rectifying potassium channels, glial cells, astrocytes, oligodendrocytes, resting membrane potential, potassium buffering, glutamate homeostasis, seizures, white matter pathology, cell cycle regulation, gliosis, high-grade glioma, temporal lobe epilepsy, amyotrophic lateral sclerosis, retinal degeneration, therapeutic target
- MeSH terms
- Kcnj10 Channel, Animals, Buffers, Cell Differentiation, Humans, Membrane Potentials, Neuroglia, Potassium, Potassium Channels, Inwardly Rectifying
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