The role of osmotic pressure and membrane potential in K(+)-stimulated taurine release from cultured astrocytes and LRM55 cells

Abstract

The effects of [K+]o on taurine release from glial cells were studied with primary cultures of cerebellar astrocytes and with LRM55 cells, a continuous glial cell line. The characteristics of K(+)-stimulated taurine release were virtually identical in the 2 cell types. Both cerebellar astrocytes and LRM55 cells released taurine when stimulated with high-K+ medium prepared by isosmotically substituting KCl for NaCl, but neither cell type released taurine when stimulated with hyperosmotic high-K+ medium prepared by adding solid KCl to control medium. The membrane potential of LRM55 cells was measured by intracellular recording and was insensitive to changes in [K+]o below 20 mM. LRM55 cells released taurine when stimulated with nondepolarizing concentrations of K+ (13-22 mM) if the isosmotically prepared high-K+ medium was used, but the cells did not release taurine when treated with a depolarizing concentration of K+ (50 mM) if hyperosmotic high-K+ medium was used. The time course of K(+)-stimulated taurine release was quite slow, having a time to peak of 10-15 min. Small changes (2.5-10%) in the osmolarity of the medium strongly affected taurine release by cerebellar astrocytes and LRM55 cells. K(+)-stimulated taurine release from both cell types was inhibited when the osmolarity was increased with sucrose or NaCl and was enhanced when the osmolarity was reduced. Similarly, baseline taurine release was suppressed by small elevations in osmolarity and increased by reduced osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)

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

“…The C1-dependence of the high IK'I-evoked TAU release observed in Muller cells (Table 1, Fig. 2) is likewise a feature common to cerebral (Pasantes-Morales and Schousboe, 1988), and cerebellar astrocytes (Martin et al, 1990), but also cerebellar granule neurons . This C1-dependence is thought to reflect the fact that inward movement of C1-ions is a prerequisite of K'-induced cell swelling (for reviews and references, see Martin et al, 1990;Walz, 1989).…”

Ammonia-induced taurine release from cultured rabbit m�ller cells is an osmoresistant process mediated by intracellular accumulation of cyclic AMP

“…The similarities included susceptibility to changes in medium osmolarity (Martin et al, 1990b), dependence on extracellular calcium (Philibert et al, 1988), and inhibition by a potassiudchloride cotransport blocker, furosemide (Martin et al, 1990a). Thus, like in the other tissues, the release in Muller cells is understood to reflect Tau transport out of the cells with osmotically obligated water and ions via osmosensitive ion channels, as a reaction to cell swelling (see Introduction).…”

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

“…Due to its astrocytic localization in the supraoptic nucleus, the released taurine is probably of glial origin. 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).…”

“…In the supraoptic nucleus, taurine is predominantly concentrated in glial cells (Decavel & Hatton, 1995), but its role in this structure is unknown. Cultured cortical and cerebellar astrocytes have been shown to release taurine in hyposmotic solution, as well as in response to high [K¤] (Pasantes- Morales & Schousboe, 1988Holopainen, Kontro & Oja, 1989;Martin, Madelian, Seligmann & Shain, 1990). However, despite its widespread distribution and its generally accepted role as an osmoregulatory substance, the physiological participation of taurine in neuronal function is still poorly understood.…”