Dopamine d2 receptor-mediated presynaptic inhibition of olfactory nerve terminals

Olfactory receptor neurons of the nasal epithelium project via the olfactor y nerve (ON) to the glomeruli of the main olfactory bulb, where they form g lutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the olfactory bulb, and with juxtaglomerular interneur ons. The glomerular layer contains one of the largest population of dopamin e (DA) neurons in the brain, and DA in the olfactory bulb is found exclusiv ely in juxtaglomerular neurons. D2 receptors, the predominant DA receptor s ubtype in the olfactory bulb, are found in the ON and glomerular layers, an d are present on ON terminals. In the present study, field potential and si ngle-unit recordings, as well as whole cell patch-clamp techniques, were us ed to investigate the role of DA and D2 receptors in glomerular synaptic pr ocessing in rat and mouse olfactory bulb slices. DA and D2 receptor agonist s reduced ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells. Spontaneous and ON-evoked spiking of mitral cells was also reduced by DA and D2 agonists, and enhanced by D2 antagonists. DA did not produce m easurable postsynaptic changes in juxtaglomerular cells, nor did it alter t heir responses to mitral/tufted cell inputs. DA also reduced 1) paired-puls e depression of ON-evoked synaptic responses in mitral/tufted and juxtaglom erular cells and 2) the amplitude and frequency of spontaneous, but not min iature, excitatory postsynaptic currents in juxtaglomerular cells. Taken to gether, these findings are consistent with the hypothesis that activation o f D2 receptors presynaptically inhibits ON terminals. DA and D2 agonists ha d no effect in D2 receptor knockout mice, suggesting that D2 receptors are the only type of DA receptors that affect signal transmission from the ON t o the rodent olfactory bulb.