Volume‐sensitive release of taurine from cultured astrocytes: Properties and mechanism

Abstract

Release of taurine in response to cell swelling induced by hyposmolarity was observed in cultured astrocytes. Efflux of 3H-taurine increased by 30% and 70% upon reductions in osmolarity of only 5% and 10%. Reductions in osmolarity of 20%, 30%, and 50% stimulated basal taurine release by 300%, 500%, and 1,500%, respectively. The properties of this volume-sensitive release of taurine were examined to investigate: 1) its association with K+ and Cl- fluxes, currently activated during volume regulation: 2) its relationship with Ca2(+)-dependent reactions; and 3) the mechanism of the taurine efflux process. Taurine release was unaffected by removal of Na+, Ca2+, or Cl-, by pimozide and trifluoperazine, or by agents disrupting the cytoskeleton. The K+ channel inhibitors barium, quinidine, tetraethylammonium, and gadolinium had no effect. Taurine release was reduced by furosemide, a blocker of K+/Cl- cotransport, but not by the more specific inhibitor, bumetanide. It was markedly reduced by the inhibitors of Cl- channels DIDS, SITS, and anthracene-9-carboxylate. Taurine efflux was pH-dependent, being reduced at low pH values. It was decreased at 4 degrees C but not at 14 degrees C or 20 degrees C. These results suggest that the volume-sensitive release of taurine is independent of K+ fluxes but may be associated with Cl- conductances. It also seems unrelated to Ca2(+)-dependent transduction mechanisms. The Na(+)-dependent taurine carrier apparently is not involved in the swelling-induced release process.

Swelling-Induced Taurine Transport: Relationship with Chloride Channels, Anion-Exchangers and Other Swelling-Activated Transport Pathways

“…Rather, it was postulated that channels may provide a conduit for volume-activated taurine release [14,37,46]. The finding that swelling-induced taurine transport could be inhibited by the stilbene-derivative DIDS prompted the suggestion that the channels could be chloride channels [28,38,47]. Many other studies followed which showed that volume-activated taurine transport could be inhibited by other anion channels blockers.…”

Chloride current activated by hypotonicity in cultured human astrocytoma cells

“…9D and (Kimelberg & O'Connor, 1988) and increase of both potassium and chloride permeability (Medrano & Gruenstein, 1993). This depolarization shouldlead to efilux ofK+ from astrocytes, which will antagonize the proposed protective cffect of thesc cells in taking up K+ relcased by neuronal activity, an effect tcrmed 'spatial buffering' (Reichenbach, 1991 (Kimelberg et al 1990b; Pasantes-Morales, Moran & Schousboe, 1990). In cultured cerebrocortical astrocytes it was suggested that the swelling-induced current was cationic (Kimelberg et al 1990a Barres, Chun & Corey, 1990;Ritchie, 1992).…”

Agonist action of taurine on glycine receptors in rat supraoptic magnocellular neurones: possible role in osmoregulation

“…Taurine has been shown also to be released from cultured cortical and cerebellar astrocytes in response to swelling following exposure to hyposmotic solution or high extracellular potassium (Pasantes-Morales & Schousboe, 1988Holopainen et al 1989;Martin et al 1990;Kimelberg et al 1990; see Huxtable, 1992). Of particular interest is the response to hyposmotic stimuli, which can occur with minor changes in osmolarity (10-20 mosmol l¢; Martin et al 1990;Pasantes-Morales, Moran & Schousboe, 1990). Taurine is believed to be used by cells as an organic osmolyte to regulate osmotic pressure.…”