Ammonia-induced taurine release from cultured rabbit Müller cells is an osmoresistant process mediated by intracellular accumulation of cyclic AMP.
A previous study demonstrated the release of newly loaded radiolabelled taurine (Tau) from cultured rabbit Müller glia not only following typical cell volume-increasing treatments with high (65 mM) potassium ions or hypotonic media, but also with ammonium chloride (further referred to as ammonia), in a dose-dependent 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, beta-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 anion/cation 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 molecule.
Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
L
L
Faff
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A
Reichenbach
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J
Albrecht
D000641:Ammonia / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism / Q000502:physiology*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D004232:Diuretics / Q000494:pharmacology; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D005665:Furosemide / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009457:Neuroglia / Q000378:metabolism*; D009996:Osmotic Fragility / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D013654:Taurine / Q000378:metabolism*; D016875:tau Proteins / Q000378:metabolism
D004232:Diuretics; D007473:Ion Channels; D016875:tau Proteins; D013654:Taurine; D000641:Ammonia; D005665:Furosemide; D000242:Cyclic AMP; D007770:L-Lactate Dehydrogenase; D017868:Cyclic AMP-Dependent Protein Kinases; D011188:Potassium; D002118:Calcium