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Astrocytes from Na(+)-K(+)-Cl(-) cotransporter-null mice exhibit absence of swelling and decrease in EAA release.

Gui Su1, Douglas B Kintner, Michael Flagella

  • 1Department of Neurosurgery, University of Wisconsin Medical School, Madison, Wisconsin 53792, USA.

American Journal of Physiology. Cell Physiology
|April 10, 2002
PubMed
Summary
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The Na(+)-K(+)-Cl(-) cotransporter isoform 1 (NKCC1) is essential for astrocyte swelling and glutamate release in response to high extracellular potassium. NKCC1 deficiency prevents these effects, highlighting its critical role in astrocyte function.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Physiology

Background:

  • The Na(+)-K(+)-Cl(-) cotransporter isoform 1 (NKCC1) plays a role in astrocyte volume regulation.
  • Previous studies indicated NKCC1 inhibition affects astrocyte responses to high extracellular potassium ([K(+)](o)).

Purpose of the Study:

  • To investigate the role of NKCC1 in high [K(+)](o)-induced astrocyte swelling and D-aspartate release using NKCC1-deficient mice.
  • To characterize astrocyte function in the absence of NKCC1 activity.

Main Methods:

  • Utilized cortical astrocytes from NKCC1-deficient (NKCC1(-/-)) and wild-type (NKCC1(+/+)) mice.
  • Measured NKCC1 activity, intracellular chloride and sodium concentrations, cell volume changes, and D-aspartate release under varying [K(+)](o).

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Main Results:

  • NKCC1 protein and activity were absent in NKCC1(-/-) astrocytes.
  • High [K(+)](o) induced swelling and intracellular chloride accumulation in NKCC1(+/+) but not NKCC1(-/-) astrocytes.
  • Regulatory volume increase was impaired, and high [K(+)](o)-induced D-aspartate release was reduced by ~30% in NKCC1(-/-) astrocytes.

Conclusions:

  • NKCC1 is indispensable for high [K(+)](o)-induced astrocyte swelling.
  • NKCC1-mediated swelling contributes to glutamate release from astrocytes under elevated extracellular potassium conditions.