Solis J M, Herranz A S, Herreras O, Lerma J, Martin Del Rio R
Departmento Investigación, Hospital Ramón y Cajal, Madrid, Spain.
Neuroscience. 1988 Mar;24(3):885-91. doi: 10.1016/0306-4522(88)90075-9.
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.
利用透析装置在体内研究了穿通通路刺激诱发的细胞外氨基酸水平和场电位，用低氯溶液灌注大鼠齿状回。当与醋酸盐平衡时，这些灌注增强了颗粒细胞群体峰电位幅度。每当用醋酸盐溶液替代Cl-时，细胞外牛磺酸就会特异性增强，当125 mM Cl-被替代时，牛磺酸水平比基础水平增加了20倍，而其他氨基酸保持不变。然而，需要用碘化物大量替代Cl-才能使细胞外牛磺酸显著增加。用溴化物替代Cl-不会引起包括牛磺酸在内的细胞外氨基酸水平的任何变化。呋塞米是一种Cl-转运抑制剂，它极大地降低了低细胞外渗透阴离子浓度诱发的牛磺酸增加。这种药物还抑制了用9 mM K+灌注诱导的牛磺酸释放。这些发现表明，低渗透阴离子浓度诱发的细胞外牛磺酸增加可能是通过呋塞米敏感过程释放牛磺酸所致。
