In the olfactory bulb, synaptic transmission between dendrites plays an important role in the processing of olfactory information. Glutamate released from the dendrites of principal mitral cells excites the dendritic spines of granule cells, which in turn release gamma-aminobutyric acid (GABA) back onto mitral cell dendrites. Slow N-methyl-d-aspartate (NMDA) receptors on granule dendrites are particularly effective in driving this reciprocal dendrodendritic inhibition (DDI), raising the possibility that calcium influx through NMDA receptors may trigger GABA exocytosis directly. In this study, I show that NMDA receptor activation is not an absolute requirement and that DDI can be evoked solely by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors when granule cell excitability is increased or under conditions that slow AMPA receptor kinetics. In physiological extracellular Mg(2+), DDI elicited by photolysis of caged calcium in mitral dendrites is blocked by cadmium and toxins to N- and P/Q-type voltage-gated calcium channels. DDI is largely unaffected after granule dendrites have been loaded with the slow calcium chelator EGTA, suggesting a tight coupling between the site of calcium influx and the release machinery governing GABA exocytosis. These results indicate that voltage-gated calcium channels play an essential role in dendritic GABA release during reciprocal feedback inhibition in the olfactory bulb.