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Low chloride-dependent release of taurine by a furosemide-sensitive process in the In vivo rat hippocampus

1988; Elsevier BV; Volume: 24; Issue: 3 Linguagem: Inglês

10.1016/0306-4522(88)90075-9

1873-7544

José M. Solı́s, Arantxa Herranz, Óscar Herreras, Juan Lerma, Rafael Martı́n del Rı́o,

Sleep and Wakefulness Research

Abstract Extracellular amino acid levels and field potentials evoked by perforant pathway stimuli were studied in vivo by means of a dialysis device, perfusing the rat dentate gyrus with low chloride solutions. When balanced with acetate, these perfusions enhanced the granule cell population spike amplitude. A specific extracellular taurine enhancement occurred whenever Cl − was replaced by acetate solution, reaching an increase of 20-fold over the basal taurine levels when 125 mM Cl − was replaced, whereas other amino acids remained unchanged. A considerable degree of Cl − replacement with iodide was needed, however, to obtain significant increases of extracellular taurine. Perfusions with bromide instead of Cl − did not cause any change in levels of extracellular amino acids including taurine. Furosemide, an inhibitor of Cl − transport, greatly reduced the taurine increase evoked by the low extracellular concentration of permeant anions. This drug also inhibited the taurine release induced by perfusion with 9 mM K + . These findings indicate that the extracellular increase of taurine, evoked by low permeant anion concentrations, may result from the taurine release through a furosemide-sensitive process.