EFFECT OF NITROPRUSSIDE (NITRIC-OXIDE) ON ENDOGENOUS DOPAMINE RELEASE FROM RAT STRIATAL SLICES

It is becoming apparent that the synthesis of nitric oxide (NO) from L-arginine not only explains endothelium-dependent vascular relaxation, but is a widespread mechanism for the regulation of cell function and communication. We examined the role of NO on the endogenous dopamine (DA) release from rat striatum. Nitroprusside, in the concentration range of 3-100-mu-M, induced a dose-dependent increase in the endogenous DA release from rat striatal slices. The maximal response was 330% over the baseline release. A higher concentration of nitroprusside (300-mu-M) produced an inhibitory effect on the spontaneous release of DA. L-Arginine (10 and 100-mu-M), a substrate in the NO-forming enzyme system, also produced an elevation of DA release. L-Arginine-induced DA release was attenuated by N(G)-monomethyl-L-arginine, an inhibitor of NO synthase. NADPH (1-mu-M), a cofactor of NO synthase, enhanced L-arginine-induced DA release. These results suggest a possible involvement of NO in the DA release process in rat striatum.