scholarly journals Sustentacular Cell Enwrapment of Olfactory Receptor Neuronal Dendrites: An Update

Genes ◽  
2020 ◽  
Vol 11 (5) ◽  
pp. 493 ◽  
Author(s):  
Fengyi Liang
Keyword(s):  
Olfactory Receptor ◽  
Cell Types ◽  
Superficial Layer ◽  
Cell Junction ◽  
Common Belief ◽  
Apical Surface ◽  
Sustentacular Cell ◽  
Neuronal Dendrites ◽  
Sustentacular Cells ◽  
Receptor Neurons

The pseudostratified olfactory epithelium (OE) may histologically appear relatively simple, but the cytological relations among its cell types, especially those between olfactory receptor neurons (ORNs) and olfactory sustentacular cells (OSCs), prove more complex and variable than previously believed. Adding to the complexity is the short lifespan, persistent neurogenesis, and continuous rewiring of the ORNs. Contrary to the common belief that ORN dendrites are mostly positioned between OSCs, recent findings indicate a sustentacular cell enwrapped configuration for a majority of mature ORN dendrites at the superficial layer of the OE. After vertically sprouting out from the borderlines between OSCs, most of the immature ORN dendrites undergo a process of sideways migration and terminal maturation to become completely invaginated into and enwrapped by OSCs. Trailing the course of the dendritic sideways migration is the mesodendrite (mesentery of the enwrapped dendrite) made of closely apposed, cell junction connected plasma membrane layers of neighboring folds of the host sustentacular cell. Only a minority of the mature ORN dendrites at the OE apical surface are found at the borderlines between OSCs (unwrapped). Below I give a brief update on the cytoarchitectonic relations between the ORNs and OSCs of the OE. Emphasis is placed on the enwrapment of ORN dendrites by OSCs, on the sideways migration of immature ORN dendrites after emerging from the OE surface, and on the terminal maturation of the ORNs. Functional implications of ORN dendrite enwrapment and a comparison with myelination or Remak’s bundling of axons or axodendrites in the central and peripheral nervous system are also discussed.

Olfactory epithelia exhibit progressive functional and morphological defects in CF mice

2007 ◽  
Vol 293 (2) ◽  
pp. C574-C583 ◽  
Author(s):  
Barbara R. Grubb ◽  
Troy D. Rogers ◽  
Heather M. Kulaga ◽  
Kimberlie A. Burns ◽  
Robert L. Wonsetler ◽  
...  
Keyword(s):  
Olfactory Receptor ◽  
Ussing Chamber ◽  
Fold Increase ◽  
Olfactory Receptor Neurons ◽  
Sodium Absorption ◽  
Sustentacular Cells ◽  
Sensory Cilia ◽  
Morphological Defects ◽  
Receptor Neurons ◽  
Chamber Studies

In normal nasal epithelium, the olfactory receptor neurons (ORNs) are continuously replaced through the differentiation of progenitor cells. The olfactory epithelium (OE) of the cystic fibrosis (CF) mouse appears normal at birth, yet by 6 mo of age, a marked dysmorphology of sustentacular cells and a dramatic reduction in olfactory receptor neurons are evident. Electroolfactograms revealed that the odor-evoked response in 30-day-old CF mice was reduced ∼45%; in older CF mice, a ∼70% reduction was observed compared with the wild type (WT) response. Consistent with studies of CF airway epithelia, Ussing chamber studies of OE isolated from CF mice showed a lack of forskolin-stimulated Cl− secretion and an ∼12-fold increase in amiloride-sensitive sodium absorption compared with WT mice. We hypothesize that the marked hyperabsorption of Na+, most likely by olfactory sustentacular cells, leads to desiccation of the surface layer in which the sensory cilia reside, followed by degeneration of the ORNs. The CF mouse thus provides a novel model to examine the mechanisms of disease-associated loss of olfactory function.

scholarly journals Evidence of SARS-CoV2 entry protein ACE2 in the human nose and olfactory bulb

2020 ◽  
Author(s):  
M. Klingenstein ◽  
S. Klingenstein ◽  
P.H. Neckel ◽  
A. F. Mack ◽  
A. Wagner ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Epithelium ◽  
Olfactory Receptor ◽  
Respiratory Epithelium ◽  
Olfactory Receptor Neurons ◽  
Basal Cells ◽  
Sustentacular Cells ◽  
Glandular Cells ◽  
Receptor Neurons ◽  
Human Nose

ABSTRACTUsually, pandemic COVID-19 disease, caused by SARS-CoV2, presents with mild respiratory symptoms such as fever, cough but frequently also with anosmia and neurological symptom. Virus-cell fusion is mediated by Angiotensin-Converting Enzyme 2 (ACE2) and Transmembrane Serine Protease 2 (TMPRSS2) with their organ expression pattern determining viral tropism. Clinical presentation suggests rapid viral dissemination to central nervous system leading frequently to severe symptoms including viral meningitis. Here, we provide a comprehensive expression landscape of ACE2 and TMPRSS2 proteins across human, post-mortem nasal and olfactory tissue. Sagittal sections through the human nose complemented with immunolabelling of respective cell types represent different anatomically defined regions including olfactory epithelium, respiratory epithelium of the nasal conchae and the paranasal sinuses along with the hardly accessible human olfactory bulb. ACE2 can be detected in the olfactory epithelium, as well as in the respiratory epithelium of the nasal septum, the nasal conchae and the paranasal sinuses. ACE2 is located in the sustentacular cells and in the glandular cells in the olfactory epithelium, as well as in the basal cells, glandular cells and epithelial cells of the respiratory epithelium. Intriguingly, ACE2 is not expressed in mature or immature olfactory receptor neurons and basal cells in the olfactory epithelium. Similarly ACE2 is not localized in the olfactory receptor neurons albeit the olfactory bulb is positive. Vice versa, TMPRSS2 can also be detected in the sustentacular cells and the glandular cells of the olfactory epithelium.Our findings provide the basic anatomical evidence for the expression of ACE2 and TMPRSS2 in the human nose, olfactory epithelium and olfactory bulb. Thus, they are substantial for future studies that aim to elucidate the symptom of SARS-CoV2 induced anosmia of via the olfactory pathway.

Human Olfactory Receptor Neurons Express Heat Shock Protein 70: Age-Related Trends

1995 ◽  
Vol 104 (1) ◽  
pp. 47-56 ◽  
Author(s):  
Thomas V. Getchell ◽  
N. S. Rama Krishna ◽  
D. Larry Sparks ◽  
Nimrat Dhooper ◽  
Marilyn L. Getchell
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neurons ◽  
Hsp 70 ◽  
Sustentacular Cells ◽  
Age Related ◽  
Receptor Neurons

Immunocytochemical methods were used to investigate the cellular distribution and age-related trends in the expression of constitutive and/or inducible forms of heat shock protein (hsp) 70 in the human nasal mucosa of 22 subjects who ranged in age from 16 weeks prenatal to 90 years, including 3 subjects with Alzheimer's disease. The olfactory mucosa was characterized by the presence of olfactory marker protein—immunoreactive olfactory receptor neurons. The hsp 70 immunoreactivity was localized in olfactory receptor neurons and the supranuclear region of sustentacular cells in the olfactory epithelium, and in the acinar cells of the Bowman's glands in the lamina propria. A systematic age-related decrement in the expression of hsp 70 immunoreactivity was observed in the olfactory receptor neurons. This trend was not apparent in sustentacular cells and Bowman's glands. A marked decrement in hsp 70 immunoreactivity was also noted in the olfactory receptor neurons of subjects with Alzheimer's disease when compared to age-matched controls. These results suggest that the age-dependent decrease in hsp 70 in olfactory receptor neurons of older subjects and those with Alzheimer's disease may be attributable to their greater susceptibility to stress.

scholarly journals Evidence of SARS-CoV2 Entry Protein ACE2 in the Human Nose and Olfactory Bulb

2021 ◽  
pp. 1-10
Author(s):  
Moritz Klingenstein ◽  
Stefanie Klingenstein ◽  
Peter H. Neckel ◽  
Andreas F. Mack ◽  
Andreas P. Wagner ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Epithelium ◽  
Olfactory Receptor ◽  
Respiratory Epithelium ◽  
Olfactory Receptor Neurons ◽  
Basal Cells ◽  
Sustentacular Cells ◽  
Glandular Cells ◽  
Receptor Neurons ◽  
Human Nose

Usually, pandemic COVID-19 disease, caused by SARS-CoV2, presents with mild respiratory symptoms such as fever, cough, but frequently also with anosmia and neurological symptoms. Virus-cell fusion is mediated by angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) with their organ expression pattern determining viral tropism. Clinical presentation suggests rapid viral dissemination to the central nervous system leading frequently to severe symptoms including viral meningitis. Here, we provide a comprehensive expression landscape of ACE2 and TMPRSS2 proteins across human postmortem nasal and olfactory tissue. Sagittal sections through the human nose complemented with immunolabelling of respective cell types represent different anatomically defined regions including olfactory epithelium, respiratory epithelium of the nasal conchae and the paranasal sinuses along with the hardly accessible human olfactory bulb. ACE2 can be detected in the olfactory epithelium as well as in the respiratory epithelium of the nasal septum, the nasal conchae, and the paranasal sinuses. ACE2 is located in the sustentacular cells and in the glandular cells in the olfactory epithelium as well as in the basal cells, glandular cells, and epithelial cells of the respiratory epithelium. Intriguingly, ACE2 is not expressed in mature or immature olfactory receptor neurons and basal cells in the olfactory epithelium. Similarly, ACE2 is not localized in the olfactory receptor neurons albeit the olfactory bulb is positive. Vice versa, TMPRSS2 can also be detected in the sustentacular cells and the glandular cells of the olfactory epithelium. Our findings provide the basic anatomical evidence for the expression of ACE2 and TMPRSS2 in the human nose, olfactory epithelium, and olfactory bulb. Thus, they are substantial for future studies that aim to elucidate the symptom of SARS-CoV2 induced anosmia via the olfactory pathway.

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