A cursory analysis of our data might suggest to some that the genetic manipulation of the drd2 locus conferred a gross olfactory impairment to the D2R-/- mice. Rather, we argue that this is not likely because the D2R-/- mice did learn to retrieve the food pellets from the dishes and eventually learned to accurately discriminate odors. Recent electrophysiological data demonstrate that dopamine D2R's are located on glutamatergic terminal axons of olfactory nerves and depress excitatory input of the olfactory nerve to the mitral cells of the olfactory bulb [30,31]. Consequently, our data, and data from other studies, suggest that the complete lack of D2Rs in the olfactory bulb does not prevent transduction of olfactory stimuli; rather it affects the ability to habituate, or tune, olfactory nerve activity associated with repeatedly encountered concentrations of chemical stimuli [32].