Fig. 8.

A model summarizing the role of nAChRs in modulating glomerular output. The model summarizes our current state of knowledge based on this work and our previous study (D'Souza and Vijayaraghavan 2012). The arrival of cholinergic input (t = 0 s) has an excitatory effect on ET cells and mitral cells (MCs), via the activation of 4β2*-nAChRs and α3β4*-nAChRs, respectively, resulting in glutamate release onto inhibitory interneurons (green arrows). The net consequence of this excitation is a strong feedback inhibition from surrounding periglomerular (PG) cells (and perhaps, the short-axon cells). If an ON input arrives at time 0 + x seconds (the value of x to be determined), the feedback GABA release (red arrows) results in inhibition of MC output, resulting in failures upon weak stimulation. A possible locus for inhibition is ET-MC signaling (hatched green arrow). This possibility is based on our observation that slow eEPSCs on MCs are inhibited upon nAChR activation (D'Souza and Vijayaraghavan, 2012). Thus nicotinic modulation of the glomerular circuit results in an effective filtering mechanism for odor input. Modulation of direct ON-MC inputs (Najac et al. 2011) by nAChRs remains to be investigated. OSN, olfactory sensory neuron.