Figure 2.

Illustration of the nontopographical model for olfactory receptive field decorrelation. (a) Level of activation of selected MOB neurons as a function of ligand-receptor potency in its presynaptic OSN population. All response profiles depicted are from neurons innervating the same glomerulus. Negative values of neuronal activation connote inhibition. Odors with very weak potencies for the OR in question evoke no OSN activity and hence no mitral cell activity. Increasing the ligand-receptor potency to the point where it evokes OSN activity begins to excite PGo neurons, which owing to their high input resistance and small gemmule volume respond strongly to even weak inputs and deliver local intraglomerular inhibition onto mitral cells. Moderate ligand-receptor potencies begin to also directly activate mitral cells (Mi_in), but this excitation is overpowered by the inhibition received from the more strongly activated PGo neurons, which shunt away depolarizing current such that the overall net response of mitral cells (Mi_out) is inhibitory. Strong ligand-receptor potencies excite mitral cells more strongly, overwhelming the capacity of PGo inhibition to impair spike generation and hence evoking action potentials in mitral cells. The result is that mitral cells exhibit an excitatory response to high-potency odorant ligands, and an inhibitory response to odorant ligands of moderate potency – i.e., to the “surrounding” region in a space defined by odor quality, as illustrated in Figure 1c. Figure adapted from ref. [26]. (b) Illustration of the triune synapse at which an OSN excites a mitral cell and PGo cell gemmule in parallel, and the PGo cell immediately inhibits the mitral cell. This synaptic triad is the basis for nontopographical intraglomerular inhibition proposed to mediate decorrelation among similar OR receptive fields.