Characteristics of nitric oxide-evoked [H-3]taurine release from cerebral cortical neurons

Pharmacological characteristics of [H-3]taurine release evoked by nitric oxide (NO) were investigated using mouse cerebral cortical neurons in primary culture. NO generators such as S-nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) dose-dependently increased [H-3]taurine release from neurons. Such stimulatory effects of NO generators were completely abolished by hemoglobin, a NO radical scavenger, indicating that these [H-3]taurine releases might be due to NO liberated From SNAP and SNP. Sodium withdrawal from incubation buffer significantly inhibited the SNAP- and SNP-induced [H-3]taurine releases, whereas the removal of calcium showed no alterations in the [H-3]taurine release evoked by NO generators. beta-Alanine and guanidinoethane sulfonate, inhibitors of carrier-mediated taurine transport system, inhibited the SNAP-and SNP-evoked releases of [H-3] taurine in a dose-dependent manner. These results indicate that the NO-evoked [H-3]taurine release from cerebral cortical neurons is mediated by the reverse process of sodium-dependent carrier-mediated taurine transport system. Copyright (C) 1996 Elsevier Science Ltd.