Ammonia-induced taurine release from cultured rabbit müller cells is an osmoresistant process mediated by intracellular accumulation of cyclic AMP
✍ Scribed by Lidia Faff; Andreas Reichenbach; Jan Albrecht
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 707 KB
- Volume
- 46
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
A previous study demonstrated the release of newly loaded radiolabelled taurine (Tau) from cultured rabbit Miiller glia not only following typical cell volumeincreasing treatments with high (65 mM) potassium ions or hypotonic media, but also with ammonium chloride (further referred to as ammonia), in a dosedependent manner, at doses ranging from physiological (0.25 mM) to those accompanying hyperammonemic coma (5 mM) (Faff-Michalak et al., Glia 10:114-120, 1994). Stimulation of Tau release by ammonia, but not by 65 mM potassium, was correlated with a dose-dependent increase of intracellular cAMP levels. The release, as measured at 5 mM ammonia, was abolished by compounds that prevented cAMP increase: an adenylate cyclase inhibitor, miconazole, a protein kinase A inhibitor HA 1004, an anion channel blocker, niflumic acid, and a Tau transport site agonist, p-alanine. The release by ammonia differed from potassium-induced release in its resistance to 1) increase of medium tonicity by addition of 50 mM sucrose; 2) addition of the anionkation cotransport blocker, furosemide; and 3) removal of calcium from the superfusion medium. The results suggest that ammonia-induced Tau release is mediated by intracellular accumulation of cAMP and may occur either via an osmoresistant, CAMP-controlled channel or a CAMP-activated Tau transporter. The release observed at the physiological concentration of ammonium chloride suggest a role for ammonia as a signal mOkCUk.