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Cited by 55Neuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration MechanismsIon Transport and Channel Regulation

Extracellular potassium influences DNA and protein syntheses and glial fibrillary acidic protein expression in cultured glial cells

Canady, Karen S., Ali‐Osman, Francis, Rubel, Edwin W.·1990·Glia
DOI 10.1002/glia.440030508
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Abstract

Previous reports of increases in glial cell number and expression of glial fibrillary acidic protein (GFAP) in stimulated brain regions or epileptic tissue have implicated a role for increases in extracellular potassium concentration ([K+]o) in glial reactions. We examined the effects of altered [K+]o on DNA and protein syntheses and GFAP expression of cultured glial cells isolated from the posthatch chick brain stem. [K+]o was varied by adding both KCl and NaCl to K+, NaCl‐free medium to achieve final [K+] of 1–50 mM. DNA and protein syntheses were measured by incorporation of 3 H‐thymidine and 3 H‐leucine, respectively, into acid‐insoluble material. GFAP expression was measured by a dot‐immunoblotting assay. DNA synthesis in glial cells cultured in high (5–50 mM) K+o was 45–60% less than that of cells cultured in low (1–3 mM) K+o. Protein synthesis per cell was increased 34–44% in cells cultured in high K+ as compared to those cultured in low K+. GFAP expression was inversely related to [K+]o over the 1–10 mM range. Compared to the baseline of 3 mM K+o, GFAP per cell was increased 65% at 1 mM and decreased 45% at 10 mM. These data suggest that increases in glial cell number and GEAP immunoreactivity found in sites of increased neuronal activity and in pathological tissues may not be caused solely by persistent increases in [K+]o. Instead, these results suggest that neuronal activity, through the release of K+, may have an inhibitory influence on glial proliferation and GFAP expression. In light of work by others implying a relationship between GFAP immunoreactivity and rigidity of astroglial processes together with the data presented here, we suggest that the elevated [K+]o accompanying neuronal activity, by inhibiting GFAP expression, may facilitate the morphological plasticity of glial cells. Conversely, conditions of low [K+]o may contribute to rigidity of astrocytic processes.

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Crossref · 10.1002/glia.440030508

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  • Membrane hyperpolarization at the G1/S checkpoint is generally required for S phase initiation.

    “A number of studies suggest that membrane hyperpolarization at the G1/S checkpoint is generally required for S phase initiation.”

    From Membrane potential and cancer progression (2013) · cites this paper as Canady et al., 1990

  • Depolarizing the cell membrane halts G1/S progression in glia, Schwann cells, lymphocytes, V79 Chinese hamster lung cells, C1300 mouse neuroblastoma cells, and MCF-7 human breast cancer cells.

    “For example, depolarizing the cell membrane halts G1/S progression in glia (Canady et al., 1990), Schwann cells (Wilson and Chiu, 1993), lymphocytes (Price et al., 1989; Freedman et al., 1992; Wang et al., 1992), V79 Chinese hamster lung cells (Sachs et al., 1974), C1300 mouse neuroblastoma cells (Boonstra et al., 1981), and MCF-7 human breast cancer cells (Wonderlin et al., 1995).”

    From Membrane potential and cancer progression (2013) · cites this paper as Canady et al., 1990

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Authors
Canady, K. S., Ali‐Osman, F., & Rubel, E. W.
Affiliations
University of Washington (US)
Corresponding author
Rubel, Edwin W.
ORCID
Rubel, Edwin W.
Venue
Glia
Publisher
Wiley
Published
1990-01
Volume
3
Issue
5
Pages
368-374
ISSN
  • 0894-1491 (ISSN-L)
  • 1098-1136
DOI
10.1002/glia.440030508
OpenAlex
W2102067114
Cited by
55
References
42
Citations by year
2023: 1 · 2022: 1 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 2 · 2016: 2 · 2014: 1 · 2013: 2
FWCI
0.98
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 5398 d)
Locations
  • Glia (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5t32gm007108-40)
  • National Institute on Deafness and Other Communication Disorders (DC 00393)
  • National Institute of General Medical Sciences (GM-07108)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
extracellular potassium, glial fibrillary acidic protein, glial cell proliferation, DNA synthesis, protein synthesis, astrocytes, neuronal activity, potassium release, glial plasticity
MeSH terms
Animals, Cells, Cultured, DNA, Extracellular Space, Glial Fibrillary Acidic Protein, Nerve Tissue Proteins, Neuroglia, Potassium

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