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Ion channel expression and function in astrocytic scars

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Molecular Signaling and Regulation in Glial Cells

Abstract

We have studied electrophysiological properties of glial cells undergoing injury induced proliferation using whole-cell patch-clamp recordings. Mechanical injury to confluent monolayers of spinal cord astrocytes resulted in a transient induction of cell proliferation that lasted for approximately 48h. Astrocytic scars healed by both re-growth into the scar region and by recruitment of newly formed cells. The in vitro scar resembled reactive gliosis in many respects including increased expression of GFAP. Cell proliferation was a requirement in the scar healing response and mitogen inhibitors such as cytosinearabinoside (Ara-C) retarded scar healing. Cells actively dividing at the scar differed absolutely in their electrophysiology from uninjured astrocytes on the same coverslip but over 300 p,m distant from the scar. Proliferating “scarring” cells had resting membrane potentials of ~ -55 mV and expressed large outwardly rectifying K+ currents but mostly lacked inwardly rectifying K+ currents. They also expressed prominent voltage-activated Na+ currents. By contrast non-dividing astrocytes that were not associated with the scar had more negative resting potentials ~ -70 mV, expressed predominantly inwardly rectifying K+ currents and most cells lacked Na+ currents. Inhibition of outward K+ currents by 2 mM 4-aminopyridine (4-AP) inhibited astrocyte proliferation and prevented scar healing suggesting that the up-regulation of 4-AP sensitive K+ channels is necessary for injury induced proliferation.

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© 1997 Springer-Verlag Berlin Heidelberg

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Sontheimer, H., Fernandez-Marques, E. (1997). Ion channel expression and function in astrocytic scars. In: Jeserich, G., Althaus, H.H., Richter-Landsberg, C., Heumann, R. (eds) Molecular Signaling and Regulation in Glial Cells. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60669-4_10

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  • DOI: https://doi.org/10.1007/978-3-642-60669-4_10

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64501-3

  • Online ISBN: 978-3-642-60669-4

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