Despite the importance of somatodendritic dopamine (DA) release in the Substantia Nigra pars compacta (SNc), its mechanism remains poorly understood. Using a novel approach combining fast-scan controlled-adsorption voltammetry (FSCAV) and single-unit electrophysiology, we have investigated the mechanism of somatodendritic release by directly correlating basal (non-stimulated) extracellular DA concentration ([DA] ), with pharmacologically-induced changes of firing of nigral dopaminergic neurons in rat brain slices. FSCAV measurements indicated that basal [DA] in the SNc was 40.7 ± 2.0 nM (at 34 ± 0.5°C), which was enhanced by amphetamine, cocaine, and L-DOPA, and reduced by VMAT2 inhibitor, Ro4-1284. Complete inhibition of firing by TTX decreased basal [DA] , but this reduction was smaller than the effect of D receptor agonist, quinpirole. Despite similar effects on neuronal firing, the larger decrease in [DA] evoked by quinpirole was attributed to cell membrane hyperpolarization and greater reduction in cytosolic free Ca ([Ca ] ). Decreasing extracellular Ca also reduced basal [DA] , despite increasing firing frequency. Furthermore, inhibiting L-type Ca channels decreased basal [DA] , although specific Ca 1.3 channel inhibition did not affect firing rate. Inhibition of sarcoplasmic/endoplasmic reticulum Ca -ATPase (SERCA) also decreased [DA] , demonstrating the importance of intracellular Ca stores for somatodendritic release. Finally, in vivo FSCAV measurements showed that basal [DA] in the SNc was 79.8 ± 10.9 nM in urethane-anesthetized rats, which was enhanced by amphetamine. Overall, our findings indicate that although tonic somatodendritic DA release is largely independent of action potentials, basal [DA] is strongly regulated by voltage-dependent Ca influx and release of intracellular Ca .