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Altered epithelial density and expansion of bulbar projections of a discrete HSP70 immunoreactive subpopulation of rat olfactory receptor neurons in reconstituting olfactory epithelium following exposure to methyl bromide
Author(s) -
McMillan Carr Virginia,
Ring George,
Youngentob Steven L.,
Schwob James E.,
Farbman Albert I.
Publication year - 2004
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.11020
Subject(s) - biology , olfactory bulb , olfactory epithelium , lesion , olfactory system , neuroscience , anatomy , pathology , central nervous system , medicine
A previously described subpopulation of rat olfactory receptor neurons, the 2A4(+)ORNs, is 1) distinguished by intense constitutive cytoplasmic immunoreactivity to antibodies to the 70‐kD heat shock protein (HSP70); 2) occurs sparsely but consistently through ventral and lateral olfactory epithelium (OE); and 3) projects to just two to three consistently located glomeruli in each olfactory bulb (OB) (Carr et al. [1994] J Comp Neurol 348:150–160). Immunoreactivity appears not to be stress‐related. To examine the persistence of these features following destruction and reconstitution of the OE, rats were subjected to methyl bromide‐induced OE lesion (Schwob et al. [1995] J Comp Neurol 59:15–37; Schwob et al. [1999] J Comp Neurol 412:439–457] and their OE and OBs examined with antibodies to HSP70 6–10.5 weeks postlesion. Lesioned OE showed significantly increased 2A4(+)ORN densities but no alteration of 2A4(+)ORN zonal distribution. The OBs of lesioned animals showed marked expansions of 2A4(+)ORN bulbar projections, with 2–15‐fold increases in numbers of glomeruli showing 2A4(+)axons, and projection expansions were greater in animals maintained on chronic food restriction prior to lesioning. Examination of archival 5‐month post‐MeBr lesion material indicates that altered projection patterns are maintained. J. Comp. Neurol. 469:475–493, 2004. © 2004 Wiley‐Liss, Inc.