Expression Patterns of Odorant Receptors and Response Properties of Olfactory Sensory Neurons in Aged Mice

Lee, Anderson C.; Tian, Huikai; Grosmaître, Xavier; Ma, Minghong

doi:10.1093/chemse/bjp056

Cited by 48 publications

(38 citation statements)

References 40 publications

(56 reference statements)

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“…Such shifts might also result from loss or shrinkage of neighboring glomeruli corresponding to other ORs. Indeed, OR-specific reductions in OSN number occur during aging, although zonal organization is retained (20), in accordance with our data showing the maintenance of the M72-GFP glomerulus position.…”

Section: Discussionsupporting

confidence: 92%

“…The significant loss of glomerular A:D synapses we report here is likely related to global reductions in OSN density and OR-specific OSN subpopulations (4,14,(18)(19)(20). In contrast, D:D synapses are also lost despite stability of the number of PG and mitral/tufted cells.…”

Section: Discussionmentioning

confidence: 63%

“…Although reductions of specific OSN subpopulations (20) may contribute to detection threshold deterioration, odor-induced activity patterns are maintained in the aged OE (18), as are the sensitivity and response of MOR23-GFP OSNs (20). The data suggest that morphological changes in the OE are a minor component of aging-related olfactory deficits.…”

Section: Are Morphological Changes In the Ob Related To Alterations Inmentioning

confidence: 95%

“…Some agerelated changes in the OE and OB were reported, mainly in rats (4,(14)(15)(16)(17)(18)(19)(20), but none document the kinetics of the defects. Here, we report quantitative morphometric analyses of the aging mouse OB at 2, 6, 12, 18, and 24 mo, focusing on changes in layer morphology, neuronal populations, synaptic circuitry, and OR map.…”

mentioning

confidence: 99%

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Age-induced disruption of selective olfactory bulb synaptic circuits

Richard

Taylor²,

Greer³

2010

Proc. Natl. Acad. Sci. U.S.A.

114

124

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Little is known about how normal aging affects the brain. Recent evidence suggests that neuronal loss is not ubiquitous in aging neocortex. Instead, subtle and still controversial, region-and layerspecific alterations of neuron morphology and synapses are reported during aging, leading to the notion that discrete changes in neural circuitry may underlie age-related cognitive deficits. Although deficits in sensory function suggest that primary sensory cortices are affected by aging, our understanding of the age-related cellular and molecular changes is sparse. To assess the effect of aging on the organization of olfactory bulb (OB) circuitry, we carried out quantitative morphometric analyses in the mouse OB at 2, 6, 12, 18, and 24 mo. Our data establish that the volumes of the major OB layers do not change during aging. Parallel to this, we are unique in demonstrating that the stereotypic glomerular convergence of M72-GFP OSN axons in the OB is preserved during aging. We then provide unique evidence of the stability of projection neurons and interneurons subpopulations in the aging mouse OB, arguing against the notion of an age-dependent widespread loss of neurons. Finally, we show ultrastructurally a significant layer-specific loss of synapses; synaptic density is reduced in the glomerular layer but not the external plexiform layer, leading to an imbalance in OB circuitry. These results suggest that reduction of afferent synaptic input and local modulatory circuit synapses in OB glomeruli may contribute to specific age-related alterations of the olfactory function.aging | axodendritic synapses | dendrodendritic synapses | mitral cells A ge-related neurodegenerative diseases, such as Parkinson and Alzheimer's, involve localized or widespread neuronal loss, but little is known about the changes occurring in the brain during normal aging. A growing consensus argues against widespread neuronal loss and atrophy during aging (1, 2). Rather, subtle region-and layer-specific alterations of neuronal morphology and synaptic connections are reported in the neocortex and hippocampus, where they may contribute to age-related cognitive deficits.The laminar organization of olfactory bulb (OB) neurons and synapses provides a simplified cortical model in which we can probe principles of neuronal and synaptic organization during aging. Sensory functions are affected by aging, including alterations in olfactory acuity, discrimination, and memory (3-12). The OB is the first central relay in the pathway processing odor information: it receives afferent input from olfactory sensory neurons (OSNs) located in the olfactory epithelium (OE) and is responsible for detecting odors in the nasal cavity. OSN axons synapse on mitral/tufted cell dendrites in OB glomerular neuropils. OB local interneurons modulate the activity of mitral/tufted cells, contributing to odor signal integration, before propagation to the piriform cortex. Projections from the OE to the OB are organized in an odor receptor (OR) map; each subpopulation of OSNs expressin...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 63%

Section: Are Morphological Changes In the Ob Related To Alterations Inmentioning

confidence: 95%

mentioning

confidence: 99%

See 2 more Smart Citations

Age-induced disruption of selective olfactory bulb synaptic circuits

Richard

Taylor²,

Greer³

2010

Proc. Natl. Acad. Sci. U.S.A.

114

124

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“…The cell densities of olfactory sensory neurons (OSNs) expressing odorant receptor (ORs) decline at advanced ages (Lee et al 2009). Following unilateral naris closure, OSNs density in the sensory-deprived side was significantly lower for some ORs as compared to the sensory-stimulated side.…”

Section: Sensory Impairment: Multiple Risk Factors Sensory Decline Inmentioning

confidence: 99%

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

Daulatzai

2016

Neurotox Res

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Sporadic Alzheimer's disease (AD) is a devastating neurodegenerative disorder. It is essential to unravel its etiology and pathogenesis. This should enable us to study the presymptomatic stages of the disease and to analyze and reverse the antemortem behavioral, memory, and cognitive dysfunction. Prima facie, an ongoing chronic vulnerability involving neural insult may lead normal elderly to mild cognitive impairment (MCI) and then to AD. Development of effective preventive and therapeutic strategies to thwart the disease pathology obviously requires a thorough delineation of underlying disruptive neuropathological processes. Our sensory capacity for touch, smell, taste, hearing, and vision declines with advancing age. Declines in different sensory attributes are considered here to be the primary "first-tier pathologies." Olfactory loss is among the first clinical signs of neurodegenerative diseases including AD and Parkinson's disease (PD). Sensory dysfunction in the aged promotes pathological disturbances in the locus coeruleus, basal forebrain, entorhinal cortex, hippocampus, and several key areas of neocortex and brainstem. Hence, sensory dysfunction is the pivotal factor that may upregulate cognitive and memory dysfunction. The age-related constellation of comorbid pathological factors may include apolipoprotein E (APOE) genotype, obesity, diabetes, hypertension, alcohol abuse, head trauma, and obstructive sleep apnea. The concepts and trajectories delineated here are the dynamic pillars of the current hypothesis presented-it postulates that the sensory decline, in conjunction with the above pathologies, is crucial in triggering neurodegeneration and promoting cognitive/memory dysfunction in aging and AD. The application of this thesis can be important in formulating new multifactorial preventive and treatment strategies (suggested here) in order to attenuate cognitive and memory decline and ameliorate pathological dysfunction in aging, MCI, and AD.

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Chemical Senses

Elsner

2015

The Encyclopedia of Adulthood and Aging

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Chemical senses, including taste, smell, and trigeminal stimulation, are essential for safety and quality of life throughout the lifespan. Changes in aging from the physiological, cognitive, nutritional, and other realms may limit the abilities of these sensory systems, thereby increasing risk of multiple causes of morbidity. These senses are often useful in diagnosing and differentiating various pathologies.

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Expression Patterns of Odorant Receptors and Response Properties of Olfactory Sensory Neurons in Aged Mice

Cited by 48 publications

References 40 publications

Age-induced disruption of selective olfactory bulb synaptic circuits

Age-induced disruption of selective olfactory bulb synaptic circuits

Dysfunctional Sensory Modalities, Locus Coeruleus, and Basal Forebrain: Early Determinants that Promote Neuropathogenesis of Cognitive and Memory Decline and Alzheimer’s Disease

Chemical Senses

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