Olfactory marker protein modulates primary olfactory axon overshooting in the olfactory bulb

2005 ◽  
Vol 488 (1) ◽  
pp. 61-69 ◽  
Author(s):  
James A. St. John ◽  
Brian Key
1992 ◽  
Vol 115 (1) ◽  
pp. 132-136 ◽  
Author(s):  
Jon N. Kott ◽  
Haila Vickland ◽  
Xiao Ming Dong ◽  
Lesnick E. Westrum

1991 ◽  
Vol 548 (1-2) ◽  
pp. 140-148 ◽  
Author(s):  
Robin L. Smith ◽  
Harriet Baker ◽  
Kaare Kolstad ◽  
Dennis D. Spencer ◽  
Charles A. Geer

1977 ◽  
Vol 25 (12) ◽  
pp. 1311-1316 ◽  
Author(s):  
G A Monti-Graziadei ◽  
F L Margolis ◽  
J W Harding ◽  
P P Graziadei

The olfactory marker protein has been localized, by means of immunohistochemical techniques in the primary olfactory neurons of mice. The olfactory marker protein is not present in the staminal cells of the olfactory neuroepithelium, and the protein may be regarded as indicative of the functional stage of the neurons. Our data indicate that the olfactory marker protein is present in the synaptic terminals of the olfactory neurons at the level of the olfactory bulb glomeruli. The postsynaptic profiles of both mitral and periglomerular cells are negative.


1990 ◽  
Vol 104 (12) ◽  
pp. 959-964 ◽  
Author(s):  
Mayumi Inamitsu ◽  
Tadashi Nakashima ◽  
Takuya Uemura

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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