The mammalian main olfactory bulb (MOB) receives a significant noradrenergic input from the locus coeruleus. Norepinephrine (NE) is involved in the acquisition of conditioned odor preferences in neonatal animals and in some species-specific odor-dependent behaviors. Thus far, the role of NE in odor processing in adult rats remains less studied. We investigated the role of noradrenergic modulation in the MOB on odor detection and discrimination thresholds using behavioral and computational modeling approaches. Adult rats received bilateral MOB injections of vehicle, NE (0.1-1000 microM), noradrenergic receptor antagonists and NE + receptor antagonists combined. NE infusion improved odor detection and discrimination as a function of NE and odor concentration. The effect of NE on detection and discrimination magnitude at any given odor concentration varied in a non-linear function with respect to NE concentration. Receptor antagonist infusion demonstrated that alpha1 receptor activation is necessary for the modulatory effect of NE. Computational modeling showed that increases in the strength of alpha1 receptor activation leads to improved odor signal-to-noise ratio and spike synchronization in mitral cells that may underlie the behaviorally observed decrease of detection and discrimination thresholds. Our results are the first to show that direct infusion of NE or noradrenergic receptor antagonists into a primary sensory network modulates sensory detection and discrimination thresholds at very low stimulus concentrations.

The mammalian main olfactory bulb receives a significant noradrenergic input from the locus coeruleus. Norepinephrine is involved in acquisition of conditioned odor preferences in neonatal animals and in some species-specific odor dependent behaviors. Thus far, the role of norepinephrine in odor processing in adult rats remains less studied. We tested the role of noradrenergic modulation in the olfactory bulb of cannulated rats by bilateral injections of vehicle (6 microL saline), the alpha noradrenergic receptor antagonist phentolamine (3.15 or 10 mM), the beta noradrenergic receptor antagonist alprenolol (12 or 120 mM), the alpha1 noradrenergic receptor antagonist prazosin (1 or 10(-2) mM) and the alpha2 noradrenergic receptor antagonist yohimbine (2 or 0.02 mM) 20 min before two different behavioral tasks. We found that local blockade of noradrenergic receptors in the olfactory bulb did not affect the formation of habituation memory to an odorant over sequential presentations separated by 5-min intertrial intervals. However, spontaneous discrimination between chemically related odorants was impaired when noradrenergic receptors, and in particular alpha1 receptors, were blocked by local antagonist infusion into the olfactory bulb. By contrast, discrimination was improved when beta receptors were blocked. These results show that although the formation of a habituation memory to odorants is not affected by noradrenergic modulation, the specificity of this memory is affected. In contrast, reward-motivated discrimination learning was not impaired, but slowed down in rats in which both alpha and beta receptors had been blocked.