Postnatal Odor Exposure Increases the Strength of Interglomerular Lateral Inhibition onto Olfactory Bulb Tufted Cells.

Abstract

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.