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

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 microM 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 microM diltiazem and when Ca2+ was replaced by Co2+. The rate of spontaneous release increased slowly and continually when Co2+ was substituted for Ca2+ 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 antagonistic metal ions were replaced with Ca2+ and when organic channel blockers were removed.