Respiratory and sniffing behaviors throughout adulthood and aging in mice

Wesson, Daniel W.; Varga-Wesson, Adrienn G.; Borkowski, Anne H.; Wilson, Donald A.

doi:10.1016/j.bbr.2011.04.016

Cited by 19 publications

(11 citation statements)

References 55 publications

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“…This is also in accordance with a number of previous studies performed in rodents exposed to a novel olfactory cue (Kepecs et al 2007;Macrides et al 1982;Welker 1964;Wesson et al 2008;Youngentob et al 1987). In fact, even age-related pathologies known to induce olfactory deficits do not affect sniffing patterns induced by exposure to novel odors (Wesson et al 2011). Whether in physiological or pathological contexts, the sniffing frequency pattern for a novel odor is stereotyped and highly stable.…”

Section: Insulin and Glucose Suppress Discrimination Ability While Mgsupporting

confidence: 92%

“…Sampling a novel odorant results in reliable induction of high-frequency (6-10 Hz) sniffing (Kepecs et al 2007;Macrides et al 1982;Welker 1964;Wesson et al 2008;Youngentob et al 1987). Habituation induced by odor repetition leads to a decrease in orientation responses (Sundberg et al 1982) and sniffing frequency (Wesson et al 2011). In this sense, respiratory activity can be a good index of-(i) stimulus novelty detection, (ii) odor habituation or adaptation to the environment, or (iii) olfactory discrimination (Kepecs et al 2007;Ranade et al 2013;Rojas-Libano et al 2014;Uchida and Mainen 2003;Welker 1964;Youngentob et al 1987).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of olfactory-driven behavior by metabolic signals: role of the piriform cortex

et al. 2018

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Olfaction is one of the major sensory modalities that regulates food consumption and is in turn regulated by the feeding state. Given that the olfactory bulb has been shown to be a metabolic sensor, we explored whether the anterior piriform cortex (aPCtx)-a higher olfactory cortical processing area-had the same capacity. Using immunocytochemical approaches, we report the localization of Kv1.3 channel, glucose transporter type 4, and the insulin receptor in the lateral olfactory tract and Layers II and III of the aPCtx. In current-clamped superficial pyramidal (SP) cells, we report the presence of two populations of SP cells: glucose responsive and non-glucose responsive. Using varied glucose concentrations and a glycolysis inhibitor, we found that insulin modulation of the instantaneous and spike firing frequency are both glucose dependent and require glucose metabolism. Using a plethysmograph to record sniffing frequency, rats microinjected with insulin failed to discriminate ratiometric enantiomers; considered a difficult task. Microinjection of glucose prevented discrimination of odorants of different chain-lengths, whereas injection of margatoxin increased the rate of habituation to repeated odor stimulation and enhanced discrimination. These data suggest that metabolic signaling pathways that are present in the aPCtx are capable of neuronal modulation and changing complex olfactory behaviors in higher olfactory centers.

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Section: Insulin and Glucose Suppress Discrimination Ability While Mgsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Modulation of olfactory-driven behavior by metabolic signals: role of the piriform cortex

et al. 2018

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“…Control over sniffing may be particularly important for limiting the access of highly intense odors to the nose, as the capacity for differentiation among odors is sharply reduced when odorants are extremely strong. The regulation of sampling behaviors (sniffing, antennal flicking) and their role in perception is an ongoing field of research (Koehl, 2006 ; Carey et al, 2009 ; Shusterman et al, 2011 ; Wesson et al, 2011 ).…”

Section: Addressing the Problem Of Concentration Invariancementioning

confidence: 99%

Sequential mechanisms underlying concentration invariance in biological olfaction

Cleland¹,

Chen²,

Hozer³

et al. 2012

Front. Neuroeng.

122

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Concentration invariance—the capacity to recognize a given odorant (analyte) across a range of concentrations—is an unusually difficult problem in the olfactory modality. Nevertheless, humans and other animals are able to recognize known odors across substantial concentration ranges, and this concentration invariance is a highly desirable property for artificial systems as well. Several properties of olfactory systems have been proposed to contribute to concentration invariance, but none of these alone can plausibly achieve full concentration invariance. We here propose that the mammalian olfactory system uses at least six computational mechanisms in series to reduce the concentration-dependent variance in odor representations to a level at which different concentrations of odors evoke reasonably similar representations, while preserving variance arising from differences in odor quality. We suggest that the residual variance then is treated like any other source of stimulus variance, and categorized appropriately into “odors” via perceptual learning. We further show that naïve mice respond to different concentrations of an odorant just as if they were differences in quality, suggesting that, prior to odor categorization, the learning-independent compensatory mechanisms are limited in their capacity to achieve concentration invariance.

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“…To achieve this, we monitored respiration for changes (or lack thereof) in odor-evoked sniffing which is reflexively displayed by rodents upon detection of a novel stimulus. To monitor sniffing, we adapted a plethysmograph and olfactometer based upon the methods of Wesson et al (2011) and Youngentob (2005) and delivered animals progressively increasing intensities of odor vapors in an ascending stair-case design. These results, which sensitively and rigorously define odor detection sensitivity deficits following OB injections of PFFs, add to our understanding of the pathological mechanisms of olfactory deficits in PD.…”

Section: Introductionmentioning

confidence: 99%

Deficits in olfactory sensitivity in a mouse model of Parkinson’s disease revealed by plethysmography of odor-evoked sniffing

Johnson

Bergkvist

Mercado

et al. 2020

Preprint

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Hyposmia is evident in over 90% of Parkinson’s disease (PD) patients. A characteristic of PD is intraneuronal deposits composed in part of α-synuclein fibrils. Based on the analysis of post-mortem PD patients, Braak and colleagues suggested that early in the disease α-synuclein pathology is present in the dorsal motor nucleus of the vagus, as well as the olfactory bulb and the anterior olfactory nucleus, and then later affects other interconnected brain regions. Here, we bilaterally injected α-synuclein preformed fibrils into the olfactory bulb of wild type male and female mice. Six-months after injection, the anterior olfactory nucleus and the piriform cortex displayed a high α-synuclein pathology load. We evaluated olfactory perceptual function by monitoring odor-evoked sniffing behavior in a plethysmograph at one-, three- and six-months after injection of α-synuclein fibrils. At all-time points, females injected with fibrils exhibited reduced odor detection sensitivity, which was detectable with the semi-automated plethysmography apparatus, but not a buried pellet test. In future studies, this sensitive methodology we used to assess olfactory detection deficits could be used to define how α-synuclein pathology affects other aspects of olfactory perception in PD models and to clarify the neuropathological underpinnings of these deficits.Highlights- α-synuclein pathology spreads through neuronally-connected areas after bilateral injection of preformed fibrils into the olfactory bulb.- A plethysmograph and an olfactometer were used for a semi-automated screen of odor-evoked sniffing as an assay for odor detection sensitivity.- Bilateral olfactory bulb injections of α-synuclein preformed fibrils in female mice led to reduced sensitivity for detecting odors.- The semi-automated plethysmography apparatus was more sensitive at detecting odor detection deficits than the buried pellet test.

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Respiratory and sniffing behaviors throughout adulthood and aging in mice

Cited by 19 publications

References 55 publications

Modulation of olfactory-driven behavior by metabolic signals: role of the piriform cortex

Modulation of olfactory-driven behavior by metabolic signals: role of the piriform cortex

Sequential mechanisms underlying concentration invariance in biological olfaction

Deficits in olfactory sensitivity in a mouse model of Parkinson’s disease revealed by plethysmography of odor-evoked sniffing

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