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Properties and glial origin of osmotic‐dependent release of taurine from the rat supraoptic nucleus
Author(s) -
Deleuze Charlotte,
Duvoid Anne,
Hussy Nicolas
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.463bt.x
Subject(s) - taurine , osmotic concentration , supraoptic nucleus , osmoregulation , medicine , dids , tonicity , endocrinology , vasopressin , chemistry , glycine receptor , extracellular , osmoreceptor , biophysics , biology , biochemistry , glycine , amino acid , ecology , salinity , membrane
1 Taurine, prominently concentrated in glial cells in the supraoptic nucleus (SON), is probably involved in the inhibition of SON vasopressin neurones by peripheral hypotonic stimulus, via activation of neuronal glycine receptors. We report here the properties and origin of the osmolarity‐dependent release of preloaded [ 3 H]taurine from isolated whole SO nuclei. 2 Hyposmotic medium induced a rapid, reversible and dose‐dependent increase in taurine release. Release showed a high sensitivity to osmotic change, with a significant enhancement with less than a 5 % decrease in osmolarity. Hyperosmotic stimulus decreased basal release. 3 Evoked release was independent of extracellular Ca 2+ and Na + , and was blocked by the Cl − channel blockers DIDS (4,4′‐diisothiocyanatostilbene‐2,2′‐disulphonic acid) and DPC ( N‐ phenylanthranilic acid), suggesting a diffusion process through volume‐sensitive Cl − channels. 4 Evoked release was transient for large osmotic reductions (≥ 15 %), probably reflecting regulatory volume decrease (RVD). However, it was sustained for smaller changes, suggesting that taurine release induced by physiological variations in osmolarity is not linked to RVD. 5 Basal and evoked release were strongly inhibited by an incubation of the tissue with the glia‐specific toxin fluorocitrate, but were unaffected by a neurotoxic treatment with NMDA, demonstrating the glial origin of the release of taurine in the SON. 6 The high osmosensitivity of taurine release suggests an important role in the osmoregulation of the SON function. These results strengthen the notion of an implication of taurine and glial cells in the regulation of the whole‐body fluid balance through the modulation of vasopressin release.