|
pubmed:abstractText |
The pharmacological characteristics of [3H]taurine release evoked by nitric oxide (NO) were investigated using mouse cerebral cortical neurons in primary culture. N-Methyl-D-aspartate (NMDA) and S-nitroso-N-acetylpenicillamine (SNAP) dose-dependently increased [3H]taurine release from neurons. The NMDA-evoked release of [3H]taurine was reduced to the basal level by N omega-nitro-L-arginine, a NO synthase inhibitor, and MK-801, a noncompetitive antagonist for NMDA receptors. The NMDA- and SNAP-evoked releases of [3H]taurine were completely abolished by hemoglobin, indicating that these [3H]taurine releases were evoked by NO produced by NMDA receptor activation and liberated from SNAP. Withdrawal of Na+ from incubation buffer significantly inhibited the NMDA- and SNAP-induced [3H]taurine releases, whereas removal of Ca2+ produced no alteration in the SNAP-evoked [3H]taurine release. In addition, beta-alanine and guanidinoethane sulfonate, antitransporters of the carrier-mediated taurine transport system, reduced the NMDA- and SNAP-evoked releases of [3H]taurine in a dose-dependent manner. These results indicate that the NO-evoked [3H]taurine release from cerebral cortical neurons is mediated by a reversal of the Na(+)-dependent carrier-mediated taurine transport system.
|
