Abstract
Dopamine (DA) neurons release DA not only from axon terminals at the striatum, but from their somata and dendrites at the substantia nigra pars compacta (SNc). Released DA may auto-regulate further DA release or modulate non-DA cells. However, the actual mechanism of somatodendritic DA release, especially the Ca2+ dependency of the process, remains controversial. In this study, we used amperometry to monitor DA release from somata of acutely isolated rat DA neurons. We found that DA neurons spontaneously released DA in the resting state. Removal of extracellular Ca2+ and application of blockers for voltage-operated Ca2+ channels (VOCCs) suppressed the frequency of secretion events. Activation of VOCCs by stimulation with K+-rich saline increased the frequency of secretion events, which were also sensitive to blockers for L- and T-type Ca2+ channels. These results suggest that Ca2+ influx through VOCCs regulates DA release from somata of DA neurons.
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