Roles of two types of anion channels in glutamate release from mouse astrocytes under ischemic or osmotic stress

Roles of two types of anion channels in glutamate release from mouse astrocytes under ischemic or... Astrocytes release glutamate upon hyperexcitation in the normal brain, and in response to pathologic insults such as ischemia and trauma. In our experiments, both hypotonic and ischemic stimuli caused the release of glutamate from cultured mouse astrocytes, which occurred with little or no contribution of gap junction hemichannels, vesicle‐mediated exocytosis, or reversed operation of the Na‐dependent glutamate transporter. Cell swelling and chemical ischemia activated, in cell‐attached membrane patches, anionic channels with large unitary conductance (∼400 pS) and inactivation kinetics at potentials more positive than +20 mV or more negative than −20 mV. These properties are different from those of volume‐sensitive outwardly rectifying (VSOR) Cl− channels, which were also expressed in these cells and exhibited intermediate unitary conductance (∼80 pS) and inactivation kinetics at large positive potentials of more than +40 mV. Both maxi‐anion channels and VSOR Cl− channels were permeable to glutamate with permeability ratios of glutamate to chloride of 0.21 ± 0.07 and 0.15 ± 0.01, respectively. However, the release of glutamate was significantly more sensitive to Gd3+, a blocker of maxi‐anion channels, than to phloretin, a blocker of VSOR Cl− channels. We conclude that these two channels jointly represent a major conductive pathway for the release of glutamate from swollen and ischemia‐challenged astrocytes, with the contribution of maxi‐anion channels being predominant. © 2006 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Roles of two types of anion channels in glutamate release from mouse astrocytes under ischemic or osmotic stress

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Publisher
Wiley
Copyright
Copyright © 2006 Wiley‐Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
DOI
10.1002/glia.20400
pmid
16883573
Publisher site
See Article on Publisher Site

Abstract

Astrocytes release glutamate upon hyperexcitation in the normal brain, and in response to pathologic insults such as ischemia and trauma. In our experiments, both hypotonic and ischemic stimuli caused the release of glutamate from cultured mouse astrocytes, which occurred with little or no contribution of gap junction hemichannels, vesicle‐mediated exocytosis, or reversed operation of the Na‐dependent glutamate transporter. Cell swelling and chemical ischemia activated, in cell‐attached membrane patches, anionic channels with large unitary conductance (∼400 pS) and inactivation kinetics at potentials more positive than +20 mV or more negative than −20 mV. These properties are different from those of volume‐sensitive outwardly rectifying (VSOR) Cl− channels, which were also expressed in these cells and exhibited intermediate unitary conductance (∼80 pS) and inactivation kinetics at large positive potentials of more than +40 mV. Both maxi‐anion channels and VSOR Cl− channels were permeable to glutamate with permeability ratios of glutamate to chloride of 0.21 ± 0.07 and 0.15 ± 0.01, respectively. However, the release of glutamate was significantly more sensitive to Gd3+, a blocker of maxi‐anion channels, than to phloretin, a blocker of VSOR Cl− channels. We conclude that these two channels jointly represent a major conductive pathway for the release of glutamate from swollen and ischemia‐challenged astrocytes, with the contribution of maxi‐anion channels being predominant. © 2006 Wiley‐Liss, Inc.

Journal

GliaWiley

Published: Oct 1, 2006

References

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