Non-cell autonomous OTX2 in the piriform cortex regulates parvalbumin cell maturation states and olfactory-driven behavior

Abstract

AbstractThe timing of critical periods of juvenile brain plasticity is driven by the maturation of parvalbumin interneurons in the neocortex, a process regulated in part by non-cell autonomous activity of the OTX2 homeoprotein transcription factor. However, the involvement of critical periods in olfactory paleocortex maturation is unknown. Here, we find that the adult mouse piriform cortex parvalbumin interneurons display particularly low molecular maturation that increases in aged animals. Expression analysis of a large panel of genes reveals that an acute increase in piriform cortex OTX2 levels in young adult mice increasesPvalbexpression as well asAdamts9expression, resulting in increased extracellular perineuronal net levels, while reducing OTX2 transfer decreasesPvalbexpression and increasesMmp9expression, resulting in decreased perineuronal net levels. Reduction in OTX2 also stimulates odor-driven cFos activity in piriform cortex parvalbumin cells and disrupts olfactory-driven behavior. Our findings suggest plasticity in piriform cortex involves OTX2 activity on parvalbumin cells and lacks strictly defined critical periods.