Mechanisms governing dendritic gamma-aminobutyric acid (GABA) release in the rat olfactory bulb

In the olfactory bulb, synaptic transmission between dendrites plays an imp ortant role in the processing of olfactory information. Glutamate released from the dendrites of principal mitral cells excites the dendritic spines o f 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 den drodendritic 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 th at DDI can be evoked solely by alpha -amino-3-hydroxy-5-methyl-4-isoxazolep ropionic acid (AMPA) receptors when granule cell excitability is increased or under conditions that slow AMPA receptor kinetics. In physiological extr acellular Mg2+, DDI elicited by photolysis of caged calcium in mitral dendr ites is blocked by cadmium and toxins to N- and P/Q-type voltage-gated calc ium channels. DDI is largely unaffected after granule dendrites have been l oaded with the slow calcium chelator EGTA, suggesting a tight coupling betw een the site of calcium influx and the release machinery governing GABA exo cytosis. These results indicate that voltage-gated calcium channels play an essential role in dendritic GABA release during reciprocal feedback inhibi tion in the olfactory bulb.