Abstract:
: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.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Faff L,Reichenbach A,Albrecht Jdoi
10.1002/(SICI)1097-4547(19961015)46:2<231::AID-JNRsubject
Has Abstractpub_date
1996-10-15 00:00:00pages
231-8issue
2eissn
0360-4012issn
1097-4547pii
10.1002/(SICI)1097-4547(19961015)46:2<231::AID-JNRjournal_volume
46pub_type
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