CHARACTERISTICS OF NITRIC OXIDE-EVOKED [H-3] TAURINE RELEASE FROM CEREBRAL CORTICAL-NEURONS

Pharmacological characteristics of [H-3]taurine release evoked by nitr ic oxide (NO) were investigated using mouse cerebral cortical neurons in primary culture. NO generators such as S-nitroso-N-acetylpenicillam ine (SNAP) and sodium nitroprusside (SNP) dose-dependently increased [ H-3]taurine release from neurons. Such stimulatory effects of NO gener ators were completely abolished by hemoglobin, a NO radical scavenger, indicating that these [H-3]taurine releases might be due to NO libera ted From SNAP and SNP. Sodium withdrawal from incubation buffer signif icantly inhibited the SNAP- and SNP-induced [H-3]taurine releases, whe reas the removal of calcium showed no alterations in the [H-3]taurine release evoked by NO generators. beta-Alanine and guanidinoethane sulf onate, inhibitors of carrier-mediated taurine transport system, inhibi ted the SNAP-and SNP-evoked releases of [H-3] taurine in a dose-depend ent manner. These results indicate that the NO-evoked [H-3]taurine rel ease from cerebral cortical neurons is mediated by the reverse process of sodium-dependent carrier-mediated taurine transport system. Copyri ght (C) 1996 Elsevier Science Ltd.