Renewing olfactory receptor neurons in goldfish do not require contact with the olfactory bulb to develop normal chemical responsiveness

1997 ◽  
Vol 181 (5) ◽  
pp. 425-437 ◽  
Author(s):  
H. P. Zippel ◽  
A. Hansen ◽  
J. Caprio
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neurons ◽  
Receptor Neurons

scholarly journals Accumulation of stress-related proteins within the glomeruli of the rat olfactory bulb following damage to olfactory receptor neurons

2008 ◽  
Vol 71 (4) ◽  
pp. 265-277 ◽  
Author(s):  
Kazuho Hirata ◽  
Takaaki Kanemaru ◽  
Motozumi Minohara ◽  
Akinobu Togo ◽  
Jun-ichi Kira
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neurons ◽  
Receptor Neurons ◽  
Related Proteins

Highly Specific Olfactory Receptor Neurons for Types of Amino Acids in the Channel Catfish

2007 ◽  
Vol 98 (4) ◽  
pp. 1909-1918 ◽  
Author(s):  
Alexander A. Nikonov ◽  
John Caprio
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Neutral Amino Acid ◽  
Olfactory Receptor Neurons ◽  
Side Chain ◽  
Single Group ◽  
Group I ◽  
Receptor Neurons

Odorant specificity to l-α-amino acids was determined electrophysiologically for 93 single catfish olfactory receptor neurons (ORNs) selected for their narrow excitatory molecular response range (EMRR) to only one type of amino acid (i.e., Group I units). These units were excited by either a basic amino acid, a neutral amino acid with a long side chain, or a neutral amino acid with a short side chain when tested at 10−7 to 10−5 M. Stimulus-induced inhibition, likely for contrast enhancement, was primarily observed in response to the types of amino acid stimuli different from that which activated a specific ORN. The high specificity of single Group I ORNs to type of amino acid was also previously observed for single Group I neurons in both the olfactory bulb and forebrain of the same species. These results indicate that for Group I neurons olfactory information concerning specific types of amino acids is processed from receptor neurons through mitral cells of the olfactory bulb to higher forebrain neurons without significant alteration in unit odorant specificity.

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.

Immunopathology of olfactory mucosa following injury to the olfactory bulb

1990 ◽  
Vol 104 (12) ◽  
pp. 959-964 ◽  
Author(s):  
Mayumi Inamitsu ◽  
Tadashi Nakashima ◽  
Takuya Uemura
Keyword(s):  
Head Injury ◽  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Neuron Specific Enolase ◽  
Olfactory Dysfunction ◽  
Olfactory Mucosa ◽  
Olfactory Receptor Neurons ◽  
Marker Protein ◽  
Olfactory Marker Protein ◽  
Receptor Neurons

AbstractRemoval of the olfactory bulb was performed on rats in an attempt to elucidate the processes of olfactory dysfunction following head injury. Degeneration and regeneration of the olfactory mucosa were examined, histopathologically and immunohistochemically. We used antisera to olfactory marker protein (OMP) and neuron specific enolase (NSE) as a marker of the mature olfactory receptor neurons. Following rapid degeneration after bulbectomy, the olfactory receptor neurons regenerated. OMP and NSE containing cells re-appeared 49 days later. However, the cell population of the neuroepithelium did not revert to the numbers observed in the non-operated neuroepithelium, even three months later. The lack of a connection between regenerated axons and the olfactory bulb may result in immature neuronal replacement and reduce the number of olfactory receptor neurons.

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