The olfactory bulb processes incoming odor signals, performing operations that include normalization and contrast enhancement, before sending information to downstream regions via mitral and tufted cell axons. Using two-photon imaging of mitral and tufted cells in vivo, the authors show that activation of raphe nuclei triggers distinct changes in these olfactory bulb output channels. Raphe stimulation sensitized tufted cells, generally enhancing odor-driven activity. On the other hand, it led to bidirectional modulation of mitral cell responses, which improved pattern separation of similar odors. The distinct effects on tufted versus mitral cells provide strong clues to functional differences between the two olfactory bulb output channels. Although the authors did not examine behavioral consequences in this study, it is tempting to speculate that these effects would simultaneously improve odor detection and discrimination.
Through an elegant series of in vitro electrophysiology, optogenetics and pharmacology experiments, the authors next dissected the cellular and synaptic mechanisms underlying the rapid changes in odor coding. They found that raphe activation exerted both excitatory and inhibitory influences on mitral and tufted cells through dual release of glutamate and serotonin, respectively. Notably, the inhibitory effects of raphe activation were polysynaptic, suggesting that serotonin may exert its direct influence on GABAergic microcircuits in the bulb.
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