Lateral inhibition between pairs of olfactory bulb (OB) mitral cells (MCs) and tufted cells (TCs) is linked to a variety of computations including gain control, decorrelation, and gamma-frequency synchronization. Differential effects of lateral inhibition onto MCs and TCs via distinct lateral inhibitory circuits are one of several recently described circuit-level differences between MCs and TCs that allow each to encode separate olfactory features in parallel. Here, using acute OB slices from mice, we tested whether lateral inhibition is affected by prior odor exposure and if these effects differ between MCs and TCs. We found that early postnatal odor exposure to the M72 glomerulus ligand acetophenone increased the strength of interglomerular lateral inhibition onto TCs, but not MCs, when the M72 glomerulus was stimulated. These increases were specific to exposure to M72 ligands because exposure to hexanal did not increase the strength of M72-mediated lateral inhibition. Therefore, early life experiences may be an important factor shaping TC odor responses.
Significance statement: Responses of olfactory (OB) bulb mitral cells (MCs) and tufted cells (TCs) are known to depend on prior odor exposure, yet the specific circuit mechanisms underlying these experience-dependent changes are unknown. Here, we show that odor exposure alters one particular circuit element, interglomerular lateral inhibition, which is known to be critical for a variety of OB computations. Early postnatal odor exposure to acetophenone, a ligand of M72 olfactory sensory neurons, increases the strength of M72-mediated lateral inhibition onto TCs, but not MCs, that project to nearby glomeruli. These findings add to a growing list of differences between MCs and TCs suggesting that that these two cell types play distinct roles in odor coding.
Keywords: electrophysiology; lateral inhibition; olfaction; olfactory bulb; plasticity.
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