On-Center/Inhibitory-Surround Decorrelation via Intraglomerular Inhibition in the Olfactory Bulb Glomerular Layer

Classical lateral inhibition, which relies on spatially ordered neural representations of physical stimuli, cannot decorrelate sensory representations in which stimulus properties are represented non-topographically. Recent theoretical and experimental studies indicate that such a non-topographical representation of olfactory stimuli predominates in olfactory bulb, thereby refuting the classical view that olfactory decorrelation is mediated by lateral inhibition comparable to that in the retina. Questions persist, however, regarding how well non-topographical decorrelation models can replicate the inhibitory “surround” that has been observed experimentally (with respect to odor feature-similarity) in olfactory bulb principal neurons, analogous to the spatial inhibitory surround generated by lateral inhibition in retina. Using two contrasting scenarios of stimulus representation – one “retinotopically” organized and one in which receptive fields are unpredictably distributed as they are in olfactory bulb – we here show that intracolumnar inhibitory interactions between local interneurons and principal neurons successfully decorrelate similar sensory representations irrespective of the scenario of representation. In contrast, lateral inhibitory interactions between these same neurons in neighboring columns are only able to effectively decorrelate topographically organized representations. While anatomical substrates superficially consistent with both types of inhibition exist in olfactory bulb, of the two only local intraglomerular inhibition suffices to mediate olfactory decorrelation

Noradrenergic and cholinergic modulation of olfactory bulb sensory processing

Neuromodulation in sensory perception serves important functions such as regulation of signal to noise ratio, attention, and modulation of learning and memory. Neuromodulators in specific sensory areas often have highly similar cellular, but distinct behavioral effects. To address this issue, we here review the function and role of two neuromodulators, acetylcholine and noradrenaline, for olfactory sensory processing in the adult main olfactory bulb. We first describe specific bulbar sensory computations, review cellular effects of each modulator and then address their specific roles in bulbar sensory processing. We finally put these data in a behavioral and computational perspective

Stressors impair odor recognition memory via an olfactory bulb-dependent noradrenergic mechanism

Non-associative habituation and odor recognition tasks have been widely used to probe questions social recognition, odor memory duration, and odor memory specificity. Among others, these paradigms have provided valuable insight into how neuromodulation, and specifically norepinephrine/noradrenaline (NE) influences odor memory. In general, NE levels are modulated by arousal, stress, and behavioral state, and there is sparse evidence of a direct relationship between NE and odor memory in adult rodents. The present study uses simple mild psychological stressors (bright light and sound), to modulate NE levels physiologically in order to probe its effect on olfactory memory. In rats with bilateral bulbar cannulations, we show that these stressors modulate olfactory memory and that this effect is at least partially mediated by olfactory bulb. Specifically, we show that the presence of stressors during the acquisition of odor memory suppresses memory for an odor when tested 30 minutes after the acquisition. This suppression is blocked by infusing NE antagonists into the olfactory bulb prior to odor acquisition. Additionally, we find that infusion of bulbar NE is sufficient to suppress odor memory in a manner mimicking that of our stressors. These effects are unlikely to be solely mediated by locomotor/exploratory changes produced by stressors, although these stressors influence certain behaviors not directly related to odor investigation. This study provides important information about how behaviorally relevant changes in NE can influence top-down sensory processing and odor memory

Blocking muscarinic receptors in the olfactory bulb impairs performance on an olfactory short term memory task

Cholinergic inputs to cortical processing networks have long been associated with attentional and top-down processing. Experimental and theoretical studies suggest that cholinergic inputs to the main olfactory bulb (OB) can modulate both neural and behavioral odor discrimination. Previous experiments from our laboratory and others demonstrate that blockade of nicotinic receptors directly impairs olfactory discrimination, whereas blockade of muscarinic receptors only measurably impairs olfactory perception when task demands are made more challenging, such as when very low-concentration odors are used or rats are required to maintain sensory memory over long durations. To further investigate the role of muscarinic signaling in the OB, we developed an olfactory delayed match-to-sample task using a digging-based behavioral paradigm. We find that rats are able to maintain robust short-term odor memory for tens to hundreds of seconds. To investigate the role of muscarinic signaling in task performance, we bilaterally infused scopolamine into the OB. We find that high dosages of scopolamine (38 mM) impair performance on the task across all delays tested, including the baseline condition with no delay, whereas lower dosages (7.6 mM and 22.8 mM) had no measureable effects. These results indicate that general execution of the match-to-sample task, even with no delay, is at least partially dependent on muscarinic signaling in the OB

Computational modeling suggests distinct, location-specific function of norepinephrine in olfactory bulb and piriform cortex

Noradrenergic modulation from the locus coerulus is often associated with the regulation of sensory signal-to-noise ratio. In the olfactory system, noradrenergic modulation affects both bulbar and cortical processing, and has been show to modulate the detection of low concentration stimuli. We here implemented a computational model of the olfactory bulb and piriform cortex, based on known experimental results, to explore how noradrenergic modulation in the olfactory bulb and piriform cortex interact to regulate odor processing. We show that as predicted by behavioral experiments in our lab, norepinephrine can play a critical role in modulating the detection and associative learning of very low odor concentrations. Our simulations show that bulbar norepinephrine serves to pre-process odor representations to facilitate cortical learning, but not recall. We observe the typical non-uniform dose – response functions described for norepinephrine modulation and show that these are imposed mainly by bulbar, but not cortical processing