Inhibitory synaptic transmission between leech heart interneurons consist of two components; graded, gated by Ca²⁺ entering via low-threshold (LVA) Ca channels, and spike-mediated, gated by Ca²⁺ entering via high-threshold (HVA) Ca channels. Changes in presynaptic background Ca²⁺ produced by Ca²⁺ influx through LVA channels does modulates spike-mediated transmission, suggesting LVA channels have access to release sites controlled by HVA channels. Here we explore whether spike-mediated and graded transmission can employ the same release sites and, thus, how Ca²⁺ influx via HVA and LVA Ca channels might interact to evoke neurotransmitter release. We recorded pre- and postsynaptic currents from voltage-clamped heart interneurons bathed in 0 mM Na⁺/5 mM Ca²⁺ saline. Employing different stimulating paradigms and inorganic Ca channels blockers, we show that strong graded synaptic transmission can occlude high-threshold/spike-mediated synaptic transmission when evoked simultaneously. Suppression of LVA Ca currents diminishes graded release and concomitantly increases the ability of Ca²⁺ entering via HVA channels to release transmitter. Uncaging of Ca chelator corroborate that graded release occludes spike-mediated. Our results indicate that both graded and spike-mediated synaptic transmission depend on the same readily releasable pool of synaptic vesicles. Thus, Ca²⁺, entering cells through different Ca channels (LVA and HVA), acts to gate release of the same synaptic vesicles. The data argue for a closer location of HVA Ca channels to release sites than LVA Ca channels. The results are summarized in a conceptual model of a heart interneuron release site.