Recent Advances in Mechanisms of Odor Perception

This paper summarizes recent findings on the olfactory system and on its functioning. Studies in molecular biology indicate that odor receptors are extremely numerous and diverse. These remarkable findings, along with recent data on the functional organization of the olfactory bulb and cortex, provide a framework for revisiting traditional views on odor coding. Both spatial and temporal neural codes seem to participate in the representation of odors in the olfactory system.

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Odor Code Sensor and Odor Reproduction

Human Olfactory Displays and Interfaces ◽

10.4018/978-1-4666-2521-1.ch024 ◽

2012 ◽

pp. 457-470

Author(s):

Kenshi Hayashi

Keyword(s):

Olfactory Bulb ◽

Odor Coding ◽

Essential Information ◽

Qualitative And Quantitative ◽

Olfactory Systems ◽

Quantitative Analyses ◽

Molecular Information ◽

Odor Receptors

In biological olfactory systems, odor receptors receive odor molecules by recognizing the molecular information. Humans can sense the odor by the signal from these activated receptors. The combination of the activated receptors is called “odor code,” and the odor codes are expressed as an “odor cluster map” of glomeruli on the olfactory bulb surface. The odor code is essential information for qualitative and quantitative analyses of odor sensation. In this chapter, development of odor sensors based on the odor code concept and an attempt to extract the parameters for odor coding from molecular informatics are described. Application of the obtained odor code for odor reproduction is also presented.

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A transformation from temporal to ensemble coding in a model of piriform cortex

10.1101/118364 ◽

2017 ◽

Cited By ~ 1

Author(s):

Merav Stern ◽

Kevin A. Bolding ◽

L.F. Abbott ◽

Kevin M. Franks

Keyword(s):

Olfactory Bulb ◽

Olfactory System ◽

Feedback Inhibition ◽

Piriform Cortex ◽

Odor Coding ◽

System A ◽

Coding Strategies ◽

Concentration Changes ◽

Recurrent Collateral ◽

The Impact

ABSTRACTDifferent coding strategies are used to represent odor information at various stages of the mammalian olfactory system. A temporal latency code represents odor identity in olfactory bulb (OB), but this temporal information is discarded in piriform cortex (PCx) where odor identity is instead encoded through ensemble membership. We developed a spiking PCx network model to understand how this transformation is implemented. In the model, the impact of OB inputs activated earliest after inhalation is amplified within PCx by diffuse recurrent collateral excitation, which then recruits strong, sustained feedback inhibition that suppresses the impact of later-responding glomeruli. Simultaneous OB-PCx recordings indicate that indeed, over a single sniff, the earliest-active OB inputs are most effective at driving PCx activity. We model increasing odor concentrations by decreasing glomerulus onset latencies while preserving their activation sequences. This produces a multiplexed cortical odor code in which activated ensembles are robust to concentration changes while concentration information is encoded through population synchrony. Our model demonstrates how PCx circuitry can implement multiplexed ensemble-identity/temporal-concentration odor coding.

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A transformation from temporal to ensemble coding in a model of piriform cortex

eLife ◽

10.7554/elife.34831 ◽

2018 ◽

Vol 7 ◽

Cited By ~ 10

Author(s):

Merav Stern ◽

Kevin A Bolding ◽

LF Abbott ◽

Kevin M Franks

Keyword(s):

Olfactory Bulb ◽

Olfactory System ◽

Feedback Inhibition ◽

Piriform Cortex ◽

Odor Coding ◽

System A ◽

Coding Strategies ◽

Concentration Changes ◽

Recurrent Collateral ◽

The Impact

Different coding strategies are used to represent odor information at various stages of the mammalian olfactory system. A temporal latency code represents odor identity in olfactory bulb (OB), but this temporal information is discarded in piriform cortex (PCx) where odor identity is instead encoded through ensemble membership. We developed a spiking PCx network model to understand how this transformation is implemented. In the model, the impact of OB inputs activated earliest after inhalation is amplified within PCx by diffuse recurrent collateral excitation, which then recruits strong, sustained feedback inhibition that suppresses the impact of later-responding glomeruli. We model increasing odor concentrations by decreasing glomerulus onset latencies while preserving their activation sequences. This produces a multiplexed cortical odor code in which activated ensembles are robust to concentration changes while concentration information is encoded through population synchrony. Our model demonstrates how PCx circuitry can implement multiplexed ensemble-identity/temporal-concentration odor coding.

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Coding of odor stimulus features among secondary olfactory structures

Journal of Neurophysiology ◽

10.1152/jn.00902.2014 ◽

2015 ◽

Vol 114 (1) ◽

pp. 736-745 ◽

Cited By ~ 6

Author(s):

Christina Z. Xia ◽

Stacey Adjei ◽

Daniel W. Wesson

Keyword(s):

Olfactory System ◽

Piriform Cortex ◽

Odor Stimulus ◽

Odor Perception ◽

Odor Coding ◽

Network Function ◽

Complex Functions ◽

Odor Exposure ◽

Stimulus Features ◽

The Brain

Sensory systems must represent stimuli in manners dependent upon a wealth of factors, including stimulus intensity and duration. One way the brain might handle these complex functions is to assign the tasks throughout distributed nodes, each contributing to information processing. We sought to explore this important aspect of sensory network function in the mammalian olfactory system, wherein the intensity and duration of odor exposure are critical contributors to odor perception. This is a quintessential model for exploring processing schemes given the distribution of odor information by olfactory bulb mitral and tufted cells into several anatomically distinct secondary processing stages, including the piriform cortex (PCX) and olfactory tubercle (OT), whose unique contributions to odor coding are unresolved. We explored the coding of PCX and OT neuron responses to odor intensity and duration. We found that both structures similarly partake in representing descending intensities of odors by reduced recruitment and modulation of neurons. Additionally, while neurons in the OT adapt to odor exposure, they display reduced capacity to adapt to either repeated presentations of odor or a single prolonged odor presentation compared with neurons in the PCX. These results provide insights into manners whereby secondary olfactory structures may, at least in some cases, uniquely represent stimulus features.

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Olfactory Optogenetics: Light Illuminates the Chemical Sensing Mechanisms of Biological Olfactory Systems

Biosensors ◽

10.3390/bios11090309 ◽

2021 ◽

Vol 11 (9) ◽

pp. 309

Author(s):

Ping Zhu ◽

Yulan Tian ◽

Yating Chen ◽

Wei Chen ◽

Ping Wang ◽

...

Keyword(s):

Olfactory Bulb ◽

Olfactory System ◽

Chemical Sensing ◽

Sensory Input ◽

Activity Patterns ◽

Neuron Activity ◽

Technical Approach ◽

Odor Coding ◽

Olfactory Systems ◽

Specific Part

The mammalian olfactory system has an amazing ability to distinguish thousands of odorant molecules at the trace level. Scientists have made great achievements on revealing the olfactory sensing mechanisms in decades; even though many issues need addressing. Optogenetics provides a novel technical approach to solve this dilemma by utilizing light to illuminate specific part of the olfactory system; which can be used in all corners of the olfactory system for revealing the olfactory mechanism. This article reviews the most recent advances in olfactory optogenetics devoted to elucidate the mechanisms of chemical sensing. It thus attempts to introduce olfactory optogenetics according to the structure of the olfactory system. It mainly includes the following aspects: the sensory input from the olfactory epithelium to the olfactory bulb; the influences of the olfactory bulb (OB) neuron activity patterns on olfactory perception; the regulation between the olfactory cortex and the olfactory bulb; and the neuromodulation participating in odor coding by dominating the olfactory bulb. Finally; current challenges and future development trends of olfactory optogenetics are proposed and discussed.

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Extinction reverses olfactory fear-conditioned increases in neuron number and glomerular size

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1505068112 ◽

2015 ◽

Vol 112 (41) ◽

pp. 12846-12851 ◽

Cited By ~ 24

Author(s):

Filomene G. Morrison ◽

Brian G. Dias ◽

Kerry J. Ressler

Keyword(s):

Olfactory Bulb ◽

Learning And Memory ◽

Olfactory Epithelium ◽

Olfactory System ◽

Structural Changes ◽

Freezing Behavior ◽

Extinction Training ◽

Odor Stimulus ◽

Main Olfactory Epithelium ◽

Odor Learning

Although much work has investigated the contribution of brain regions such as the amygdala, hippocampus, and prefrontal cortex to the processing of fear learning and memory, fewer studies have examined the role of sensory systems, in particular the olfactory system, in the detection and perception of cues involved in learning and memory. The primary sensory receptive field maps of the olfactory system are exquisitely organized and respond dynamically to cues in the environment, remaining plastic from development through adulthood. We have previously demonstrated that olfactory fear conditioning leads to increased odorant-specific receptor representation in the main olfactory epithelium and in glomeruli within the olfactory bulb. We now demonstrate that olfactory extinction training specific to the conditioned odor stimulus reverses the conditioning-associated freezing behavior and odor learning-induced structural changes in the olfactory epithelium and olfactory bulb in an odorant ligand-specific manner. These data suggest that learning-induced freezing behavior, structural alterations, and enhanced neural sensory representation can be reversed in adult mice following extinction training.

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Region-specific amyloid-β accumulation in the olfactory system influences olfactory sensory neuronal dysfunction in 5xFAD mice

Alzheimer s Research & Therapy ◽

10.1186/s13195-020-00730-2 ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Gowoon Son ◽

Seung-Jun Yoo ◽

Shinwoo Kang ◽

Ameer Rasheed ◽

Da Hae Jung ◽

...

Keyword(s):

Olfactory Bulb ◽

Sensory Neurons ◽

Olfactory System ◽

Amyloid Β ◽

Olfactory Sensory Neurons ◽

Basal Cells ◽

Irreversible Damage ◽

5Xfad Mouse ◽

Peripheral Areas ◽

5Xfad Mice

Abstract Background Hyposmia in Alzheimer’s disease (AD) is a typical early symptom according to numerous previous clinical studies. Although amyloid-β (Aβ), which is one of the toxic factors upregulated early in AD, has been identified in many studies, even in the peripheral areas of the olfactory system, the pathology involving olfactory sensory neurons (OSNs) remains poorly understood. Methods Here, we focused on peripheral olfactory sensory neurons (OSNs) and delved deeper into the direct relationship between pathophysiological and behavioral results using odorants. We also confirmed histologically the pathological changes in 3-month-old 5xFAD mouse models, which recapitulates AD pathology. We introduced a numeric scale histologically to compare physiological phenomenon and local tissue lesions regardless of the anatomical plane. Results We observed the odorant group that the 5xFAD mice showed reduced responses to odorants. These also did not physiologically activate OSNs that propagate their axons to the ventral olfactory bulb. Interestingly, the amount of accumulated amyloid-β (Aβ) was high in the OSNs located in the olfactory epithelial ectoturbinate and the ventral olfactory bulb glomeruli. We also observed irreversible damage to the ectoturbinate of the olfactory epithelium by measuring the impaired neuronal turnover ratio from the basal cells to the matured OSNs. Conclusions Our results showed that partial and asymmetrical accumulation of Aβ coincided with physiologically and structurally damaged areas in the peripheral olfactory system, which evoked hyporeactivity to some odorants. Taken together, partial olfactory dysfunction closely associated with peripheral OSN’s loss could be a leading cause of AD-related hyposmia, a characteristic of early AD.

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