Effect of arginine on basal and high potassium-induced efflux of [3H]D-aspartate from rat striatal slices.

There are conflicting reports in the literature regarding the effects of nitric oxide as well as the involvement of the cyclic GMP pathway on the transmitter release. To study the influence of the availability of the nitric oxide precursor arginine on the glutamate transmission process, rat striatal slices preloaded with the tritiated glutamate analogue D-aspartate were used. L-Arginine stimulated in a concentration-dependent way (0.01-10.0 mM) the high potassium-induced efflux of [3H]D-aspartate. The basal release was increased only by 10 mM L-arginine. Neither the basal nor the depolarization-induced efflux of [3H]D-aspartate was affected by D-arginine. The L-arginine effect was abolished by the nitric oxide synthase inhibitor L-arginine methyl ester and was not modified by cyclic GMP. Only at high concentrations of L-arginine (10 mM) could an elevation of cyclic GMP level be demonstrated. The results are discussed in terms of direct presynaptic action of nitric oxide on [3H]D-aspartate efflux and a possible modulation of glutamate release by the availability of arginine.