tex [5–7], hippocampus [8,9], and olfactory bulb [10–12] are all implicated, the cellular correlates for these processes have not been clearly delineated. The contribution of the hippocampus to olfactory memory is presently controversial [2,13–18], but is deemed unlikely for simple olfactory discrimination tasks [9,19]. In fact, the most likely candidates for a cellular correlate of olfactory memory appear to be the neuronal connections in the piriform cortex due to the associational connectivity [5] and the expression of several forms of cellular and synaptic plasticity [7,20–23].
Concerning odor discrimination itself, cellular mechanisms for this process are often attributed to the inhibitory circuitry of the olfactory bulb ([24–30]; reviewed in [31–33]). Lateral inhibitory circuits were postulated, in analogy to retina [34,35], to mediate contrast enhancement [24], for which physiological recordings [24,36,37] and modeling data, based on the well-known anatomy [29], provide additional support. Such contrast enhancement may rest in large part on the particular properties of dendrodendritic synapses between the principal output neurons (mitral cells) and local inhibitory neurons (granule cells) of the olfactory bulb. In these distinct synapses,