Hydroxylamine (0.01–30 mM), a nitric oxide (NO) generator, produced a concentration‐dependent release of [3H]dopamine ([3H]DA) from rat striatal slices. Hemoglobin (10 μM), a NO scavenger, reduced basal [3H]DA release and blocked hydroxylamine (100 μM)‐stimulated [3H]DA efflux. Tetrodotoxin (0.5 μM) had no significant effect. Sodium cyanide was used as a model compound to test the possibility that NO acted through blockade of mitochondrial electron transport. Calcium‐free experimental buffer (1 mM EGTA) reduced basal release and the hydroxylamine response, while sodium cyanide‐induced release did not change under these experimental conditions. Cadmium (200 μM), a non‐selective inhibitor of voltage‐dependent calcium channels, reduced the hydroxylamine response by 69%. Methylene blue (10 μM), an inhibitor of guanylate cyclase, produced a 3‐fold increase in the basal release but had no significant effect on the hydroxylamine response. These data suggest that NO induces calcium‐dependent [3H]DA release from the striatum via a mechanism which is independent of blockade of electron transport or activation of guanylate cyclase. © 1993 Wiley‐Liss, Inc.
- cyclic GMP
- methylene blue
- sodium cyanide
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience