Young rats prior to eye opening depend on somatosensory and olfactory function for survival, as they can learn their dam's odor and approach her without visual information. In order to establish olfactory learning, the pairing of odor and tactile stimulation is crucial. Noradrenergic activation through the locus coeruleus by a somatosensory stimulus is implicated in olfactory learning. Within the olfactory bulb (OB), the noradrenergic innervation modulates the efficacy of dendrodendritic synapses between the mitral and granule cells. At the dendrodendritic reciprocal synapses, mitral cell activity is inhibited by GABA released from the granule cells. It is noteworthy that disinhibition of the mitral cells is a crucial step in the formation of an olfactory memory. We previously showed that intrabulbar infusion of the GABA receptor antagonist, bicuculline facilitated olfactory learning. These results implicate the OB as a critical site for olfactory learning. Since the transcription factor, CREB is well known to be involved in plasticity, we examined whether CREB is involved in olfactory learning. Behavioral pharmacology shows that only long-term olfactory memory was prevented by CREB antisense infusion, but short-term memory was intact. Western blot analyses reveal that P-MAPK/ERK was increased for 1 hour after odor exposure paired with shock, followed by increase of P-CREB lasting for 6 hours. These may be evidence suggesting that synaptic plasticity in the OB underlies aversive olfactory learning. [J Physiol Sci. 2006;56 Suppl:S24]
