Properties and glial origin of osmotic‐dependent release of taurine from the rat supraoptic nucleus

Abstract

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 [3H]taurine from isolated whole SO nuclei. 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. Evoked release was independent of extracellular Ca2+ 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. 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. 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. 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.

Target cell-specific modulation of neuronal activity by astrocytes

“…This form of neuronal inhibition was proposed to depend on astrocytic calcium signaling and on activation of GABAergic interneurons, presumably by astrocytic glutamate. Another mechanism of neuronal inhibition was reported in the supraoptic nucleus: In response to a decrease of extracellular osmolarity within a physiological range, astrocytes were shown to release taurine and, thus, to activate neuronal glycine receptors (20).…”

Chloride/anion channels in glial cell membranes

“…Recent results make a glial-neuronal interaction in this sensory process very likely (Hussy et al, 1997;Deleuze et al, 1998). This mechanism will be in addition to mechanoreceptors in the membrane of SON neurons.…”

Potentiation of the glutamatergic synaptic input to rat locus coeruleus neurons by P2X7 receptors

“…In the present experiments, we found that the selective astrocytic poisons fluorocitric acid [50] and aminoadipic acid [51], most probably by interfering with the outflow of one or more than one signalling molecules, markedly depressed the BzATP-induced facilitation of sEPSCs. Both fluorocitric acid and aminoadipic acid were used at a concentration (100 μM) which was reported to interfere with the synthesis, storage and release of amino acid gliotransmitters [52,53]. Thus, we suggest that P2X7 receptors are situated at neighbouring astrocytes rather than at the nerve terminals of glutamatergic afferents innervating the LC.…”