Aging in the rat olfactory system: Relative stability of piriform cortex contrasts with changes in olfactory bulb and olfactory epithelium

1985 ◽  
Vol 235 (4) ◽  
pp. 519-528 ◽  
Author(s):  
Christine A. Curcio ◽  
Nancy A. McNelly ◽  
James W. Hinds
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Epithelium ◽  
Relative Stability ◽  
Olfactory System ◽  
Piriform Cortex

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

2015 ◽  
Vol 112 (41) ◽  
pp. 12846-12851 ◽  
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.

Chemical Factors Determine Olfactory System Beta Oscillations in Waking Rats

2007 ◽  
Vol 98 (1) ◽  
pp. 394-404 ◽  
Author(s):  
Catherine A. Lowry ◽  
Leslie M. Kay
Keyword(s):  
Olfactory Bulb ◽  
Vapor Pressure ◽  
Vapor Phase ◽  
Local Field ◽  
Olfactory System ◽  
Piriform Cortex ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Beta Oscillations ◽  
Phase Concentration

Recent studies have pointed to olfactory system beta oscillations of the local field potential (15–30 Hz) and their roles both in learning and as specific responses to predator odors. To describe odorant physical properties, resultant behavioral responses and changes in the central olfactory system that may induce these oscillations without associative learning, we tested rats with 26 monomolecular odorants spanning 6 log units of theoretical vapor pressure (estimate of relative vapor phase concentration) and 10 different odor mixtures. We found odorant vapor phase concentration to be inversely correlated with investigation time on the first presentation, after which investigation times were brief and not different across odorants. Analysis of local field potentials from the olfactory bulb and anterior piriform cortex shows that beta oscillations in waking rats occur specifically in response to the class of volatile organic compounds with vapor pressures of 1–120 mmHg. Beta oscillations develop over the first three to four presentations and are weakly present for some odorants in anesthetized rats. Gamma oscillations show a smaller effect that is not restricted to the same range of odorants. Olfactory bulb theta oscillations were also examined as a measure of effective afferent input strength, and the power of these oscillations did not vary systematically with vapor pressure, suggesting that it is not olfactory bulb drive strength that determines the presence of beta oscillations. Theta band coherence analysis shows that coupling strength between the olfactory bulb and piriform cortex increases linearly with vapor phase concentration, which may facilitate beta oscillations above a threshold.

Piriform cortex activity evoked by stimulation to olfactory bulb or olfactory epithelium in isolated ginia-pig whole brain

1998 ◽  
Vol 31 ◽  
pp. S205
Author(s):  
Takaaki Sato ◽  
Ichiro Takashima ◽  
Mutsumi Matsukawa ◽  
Kaoru Tsukada ◽  
Toshio Iijima
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Epithelium ◽  
Piriform Cortex ◽  
Whole Brain

scholarly journals Perturbation of in vivo neural activity following α-Synuclein seeding in the olfactory bulb

2020 ◽  
Author(s):  
Aishwarya S. Kulkarni ◽  
Maria del Mar Cortijo ◽  
Elizabeth R. Roberts ◽  
Tamara L. Suggs ◽  
Heather B. Stover ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Neural Activity ◽  
Olfactory System ◽  
Piriform Cortex ◽  
Field Potential ◽  
Dopamine Neurons ◽  
Motor Deficits ◽  
Wild Type ◽  
Evoked Activity

AbstractBACKGROUNDParkinson’s disease (PD) neuropathology is characterized by intraneuronal protein aggregates composed of misfolded α-Synuclein (α-Syn), as well as degeneration of substantia nigra dopamine neurons. Deficits in olfactory perception and aggregation of α-Syn in the olfactory bulb (OB) are observed during early stages of PD, and have been associated with the PD prodrome, before onset of the classic motor deficits. α-Syn fibrils injected into the OB of mice cause progressive propagation of α-Syn pathology throughout the olfactory system and are coupled to olfactory perceptual deficits.OBJECTIVEWe hypothesized that accumulation of pathogenic α-Syn in the OB impairs neural activity in the olfactory system.METHODSTo address this, we monitored spontaneous and odor-evoked local field potential dynamics in awake wild type mice simultaneously in the OB and piriform cortex (PCX) one, two, and three months following injection of pathogenic preformed α-Syn fibrils in the OB.RESULTSWe detected α-Syn pathology in both the OB and PCX. We also observed that α-Syn fibril injections influenced odor-evoked activity in the OB. In particular, α-Syn fibril-injected mice displayed aberrantly high odor-evoked power in the beta spectral range. A similar change in activity was not detected in the PCX, despite high levels of α-Syn pathology.CONCLUSIONSTogether, this work provides evidence that synucleinopathy impacts in vivo neural activity in the olfactory system at the network-level.

scholarly journals Region Specific Amyloid-β Accumulation in Olfactory Sensory Neurons Influences Ecto-Ventral Olfactory Dysfunction in 5xFAD Mice

2020 ◽  
Author(s):  
Gowoon Son ◽  
Seung-Jun Yoo ◽  
Shinwoo Kang ◽  
Ameer Rasheed ◽  
Da Hae Jung ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Sensory Neurons ◽  
Olfactory Epithelium ◽  
Olfactory System ◽  
Amyloid Β ◽  
Olfactory Dysfunction ◽  
Olfactory Sensory Neurons ◽  
Basal Cells ◽  
Irreversible Damage ◽  
5Xfad Mouse

Abstract Background: Hyposmia in Alzheimer’s disease (AD) is a typical early symptom according to numerous previous clinical studies. Although the causes of damage have been proposed in every olfactory system including olfactory epithelium, olfactory bulb and olfactory cortex, the main causes of AD- related hyposmia are largely unknown. Methods: We here focused on peripheral olfactory sensory neurons (OSNs) and delved deeper into the direct relationship between pathophysiological and behavioral results using odorants. We also histologically confirmed the pathological changes in three-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 anatomical plane. Results: We observed the odorant group, which 5xFAD mouse could not detect, also neither did physiologically activate the OSNs that propagate to the ventral olfactory bulb. Interestingly, the amount of accumulated amyloid-β (Aβ) was high in the ecto-ventrally located OSNs that showed reduced responses to odorants. We also observed irreversible damage to the ecto-region of the olfactory epithelium by measuring 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 the AD-related hyposmia, a characteristic of early AD.

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

2017 ◽  
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.

scholarly journals Perturbation of in vivo Neural Activity Following α-Synuclein Seeding in the Olfactory Bulb

2020 ◽  
Vol 10 (4) ◽  
pp. 1411-1427
Author(s):  
Aishwarya S. Kulkarni ◽  
Maria del Mar Cortijo ◽  
Elizabeth R. Roberts ◽  
Tamara L. Suggs ◽  
Heather B. Stover ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Neural Activity ◽  
Olfactory System ◽  
Piriform Cortex ◽  
Field Potential ◽  
Dopamine Neurons ◽  
Motor Deficits ◽  
Wild Type ◽  
Evoked Activity

Background: Parkinson’s disease (PD) neuropathology is characterized by intraneuronal protein aggregates composed of misfolded α-Synuclein (α-Syn), as well as degeneration of substantia nigra dopamine neurons. Deficits in olfactory perception and aggregation of α-Syn in the olfactory bulb (OB) are observed during early stages of PD, and have been associated with the PD prodrome, before onset of the classic motor deficits. α-Syn fibrils injected into the OB of mice cause progressive propagation of α-Syn pathology throughout the olfactory system and are coupled to olfactory perceptual deficits. Objective: We hypothesized that accumulation of pathogenic α-Syn in the OB impairs neural activity in the olfactory system. Methods: To address this, we monitored spontaneous and odor-evoked local field potential dynamics in awake wild type mice simultaneously in the OB and piriform cortex (PCX) one, two, and three months following injection of pathogenic preformed α-Syn fibrils in the OB. Results: We detected α-Syn pathology in both the OB and PCX. We also observed that α-Syn fibril injections influenced odor-evoked activity in the OB. In particular, α-Syn fibril-injected mice displayed aberrantly high odor-evoked power in the beta spectral range. A similar change in activity was not detected in the PCX, despite high levels of α-Syn pathology. Conclusion: Together, this work provides evidence that synucleinopathy impacts in vivo neural activity in the olfactory system at the network-level.

scholarly journals ODOR IDENTITY CAN BE EXTRACTED FROM THE RECIPROCAL CONNECTIVITY BETWEEN OLFACTORY BULB AND PIRIFORM CORTEX IN HUMANS

2021 ◽  
Author(s):  
Behzad Iravani ◽  
Artin Arshamian ◽  
Mikael Lundqvist ◽  
Leslie M Kay ◽  
Donald A Wilson ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Information Flow ◽  
Information Exchange ◽  
Olfactory System ◽  
Critical Role ◽  
Piriform Cortex ◽  
Brain Regions ◽  
Oscillatory Circuit ◽  
Healthy Human ◽  
Gamma Frequency

Neuronal oscillations route external and internal information across brain regions. In the olfactory system, the two central nodes-the olfactory bulb (OB) and the piriform cortex (PC)-communicate with each other via neural oscillations to shape the olfactory percept. Communication between these nodes have been well characterized in non-human animals but less is known about their role in the human olfactory system. Using a recently developed and validated EEG-based method to extract signals from the OB and PC sources, we show in healthy human participants that there is a bottom-up information flow from the OB to the PC in the beta and gamma frequency bands, while top-down information from the PC to the OB is facilitated by delta and theta oscillations. Importantly, we demonstrate that there was enough in-formation to decipher odor identity above chance from the low gamma in the OB-PC oscillatory circuit as early as 100ms after odor onset. These data further our understanding of the critical role of bidirectional information flow in human sensory systems to produce perception. However, future studies are needed to determine what specific odor information is extracted and communicated in the information exchange.

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

eLife ◽  
2018 ◽  
Vol 7 ◽  
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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