K+‐, hypoosmolarity‐, and NH4+‐induced taurine release from cultured rabbit Müller cells: Role of NA+ and CL− ions and relation to cell volume changes

Publisher Website
Google Scholar
Abstract
The release of preloaded radiolabeled taurine (TAU) from cultured rabbit Müller cells [14–21 days in vitro (DIV)] was measured before and after treatment with the following stimuli: (1) isoosmotic 65 mM KCI; (2) a medium made hypoosmotic by uncompensated lowering of Na+ by 40–100 mM; and 3) NH4Cl ranging from 0.25 to 5 mM. The same stimuli were tested for their effect on the cell volume by the 3-0-methyl-D-glucose (OMG) uptake method of Kletzien et al. (Anal Biochem 68:537, 1975). Hypoosmotic media and 65 mM KCl stimulated TAU release, and the release was well correlated with the increase of cell volume. The stimulatory effect of 65 mM KCI was abolished by isotonic removal of Cl− or Na+, and omission of either ion markedly enhanced the basal release of TAU. The results are roughly consistent with the characteristics of the swelling-induced TAU release reported for cultured astrocytes and neurons of various CNS regions, and also for freshly isolated, nondissociated retina. Taken together, the results are indicative of a significant role of TAU release from Müller cells, in the osmosensory response of the retina. Ammonium chloride stimulated TAU release in a dose-dependent manner, a significant stimulation being already observed at 0.5 mM, a concentration that is frequently measured in brain during acute hyperammonemia. The effect of NH4Cl was strictly chloride dependent at 0.5–2 mM, but partly Cl− independent at 5mM. The Kletzien's method did not appear to be well suited for measuring cell volume in the presence of ammonium ions. However, data from the literature on other CNS cell types plus our preliminary electron microscopic observations suggest that short-term treatments with NH4Cl at concentrations up to 1 mM are unlikely to produce cell swelling. An alternative way in which ammonium ions might trigger the “tension sensor” for TAU release is discussed. We propose that in vivo, the outward-driven TAU could counteract ammoniainduced neuronal disinhibition, according to a putative role for TAU as a gliotransmitter.