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Spontaneous and beta‐adrenergic receptor‐mediated taurine release from astroglial cells do not require extracellular calcium

Spontaneous and beta‐adrenergic receptor‐mediated taurine release from astroglial cells do not... Astroglial cells release taurine when stimulated by beta‐adrenergic agonists and other neuroactive agents. The Ca2+ ‐dependency of taurine release by an LRM55 astroglial cell line was investigated by removing Ca2+ from the perfusion medium and by using three inorganic and three organic Ca2+ ‐channel blockers (Mn2+, Co2+, Cd2+, verapamil, nifedipine, and diltiazem). Spontaneous release and release stimulated by the beta‐adrenergic agonist isoproterenol were not inhibited when cells were perfused with medium containing no added Ca2+ and 10 μM EGTA. Isoproterenol‐stimulated taurine release was not blocked when extracellular Ca2+ was completely replaced by Mn2+, Co2+, or Cd2+, nor was it blocked by verapamil, nifedipine, or diltiazem. In fact isoproterenol‐stimulated taurine release was increased by 50 μM diltiazem and when Ca2+ was replaced by Co2+. The rate of spontaneous release increased slowly and continually when Co2+ was substituted for Ca2+ or but was almost unaffected by substitution of Mn2+ or Cd2+. Application of diltiazem increased spontaneous release significantly, while verapamil and nifedipine appeared to cause small increases. These results indicate that entry of Ca2+ from the extracellular medium is not required for either receptor‐mediated or spontaneous taurine release from astroglial cells. Some other changes in the medium did strongly affect release. Both spontaneous and isoproterenol‐stimulated release were inhibited by elevated osmotic pressure, and spontaneous release was greatly increased when Ca2+ was completely removed without substituting another divalent cation. Spontaneous release increased when antagonistie metal ions were replaced with Ca2+ and when organic channel blockers were removed. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Research Wiley

Spontaneous and beta‐adrenergic receptor‐mediated taurine release from astroglial cells do not require extracellular calcium

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References (32)

Publisher
Wiley
Copyright
Copyright © 1989 Alan R. Liss, Inc.
ISSN
0360-4012
eISSN
1097-4547
DOI
10.1002/jnr.490230209
pmid
2547083
Publisher site
See Article on Publisher Site

Abstract

Astroglial cells release taurine when stimulated by beta‐adrenergic agonists and other neuroactive agents. The Ca2+ ‐dependency of taurine release by an LRM55 astroglial cell line was investigated by removing Ca2+ from the perfusion medium and by using three inorganic and three organic Ca2+ ‐channel blockers (Mn2+, Co2+, Cd2+, verapamil, nifedipine, and diltiazem). Spontaneous release and release stimulated by the beta‐adrenergic agonist isoproterenol were not inhibited when cells were perfused with medium containing no added Ca2+ and 10 μM EGTA. Isoproterenol‐stimulated taurine release was not blocked when extracellular Ca2+ was completely replaced by Mn2+, Co2+, or Cd2+, nor was it blocked by verapamil, nifedipine, or diltiazem. In fact isoproterenol‐stimulated taurine release was increased by 50 μM diltiazem and when Ca2+ was replaced by Co2+. The rate of spontaneous release increased slowly and continually when Co2+ was substituted for Ca2+ or but was almost unaffected by substitution of Mn2+ or Cd2+. Application of diltiazem increased spontaneous release significantly, while verapamil and nifedipine appeared to cause small increases. These results indicate that entry of Ca2+ from the extracellular medium is not required for either receptor‐mediated or spontaneous taurine release from astroglial cells. Some other changes in the medium did strongly affect release. Both spontaneous and isoproterenol‐stimulated release were inhibited by elevated osmotic pressure, and spontaneous release was greatly increased when Ca2+ was completely removed without substituting another divalent cation. Spontaneous release increased when antagonistie metal ions were replaced with Ca2+ and when organic channel blockers were removed.

Journal

Journal of Neuroscience Research – Wiley

Published: Jun 1, 1989

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