The anterior piriform cortex as a locus for early odor preference learning in rats

Abstract

Early odor preference learning in rats has been localized to the physiological changes in the olfactory bulb. However, the role of the olfactory cortex (e.g. the piriform cortex) was unexplored. In this work, my experiments support a critical role of the piriform cortex in early odor preference learning. First, the anterior piriform cortex (aPCX) is a critical component of early odor preference learning circuitry. Transiently silencing cells using lidocaine or muscimol local infusions in the aPCX prevents odor learning and recall. Second, acquisition of early odor preference learning in the aPCX is dependent on N-methyl-D-aspartate (NMDA) receptor activation both in vivo and in vitro. NMDARs are highly implicated in synaptic plasticity and critical in many forms of associative learning. Pups are unable to learn following local infusion of D-amino-5- phosphonopentanoate (D-APV) prior to odor conditioning. In vitro, D-APV prevents LTP induction. Third, β-adrenoceptor activation in the aPCX is required and sufficient for early odor preference learning. Stroking elicits natural norepinephrine release from the locus coeruleus to the olfactory structures including PCX. Pups cannot learn following propranolol infusions before odor conditioning. If stroking is replaced by isoproterenol infusions in the aPCX during novel odor presentations, animals will learn to prefer that odor. Fourth, odor plus stroking (OS⁺) training enhances phosphorylated cAMP response element-binding protein (pCREB), a molecule highly implicated in intracellular signalling pathways involved in learning, expression in the trained hemisphere. Finally, learning induces NMDAR subunit expression changes. At 3 hr following OS+ training, there is a significant NR1 down-regulation and at 24 hr following OS⁺ training, NR1 displays a significant up-regulation from baseline expression levels.