1995
DOI: 10.1002/cne.903590103
|View full text |Cite
|
Sign up to set email alerts
|

Reconstitution of the rat olfactory epithelium after methyl bromide‐induced lesion

Abstract: The olfactory epithelium and its neuronal population are known to have a substantial capacity to recover after either direct injury or damage to the olfactory nerve. However, the mechanisms underlying that capacity for recovery, and indeed the limits on the recovery process, are not well understood. The aim of this study is to describe in detail the way in which the olfactory epithelium reconstitutes after direct injury. Adult male rats were exposed to 330 ppm methyl bromide (MeBr) gas for a single 6-hour peri… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

25
289
2
4

Year Published

1995
1995
2005
2005

Publication Types

Select...
7

Relationship

3
4

Authors

Journals

citations
Cited by 249 publications
(325 citation statements)
references
References 53 publications
(82 reference statements)
25
289
2
4
Order By: Relevance
“…Cell division was not obviously altered at P1, P25, or adult ages. The transient increase in neurogenesis observed Ͼ1 week after the peak of cell death is consistent with delayed neurogenic responses elicited after bulbectomy or methyl bromide-induced OE lesions (Schwartz-Levy et al, 1991;Schwob et al, 1995).…”
Section: Increased Cell Death and Precursor Proliferation In ␤3gnt1supporting
confidence: 70%
“…Cell division was not obviously altered at P1, P25, or adult ages. The transient increase in neurogenesis observed Ͼ1 week after the peak of cell death is consistent with delayed neurogenic responses elicited after bulbectomy or methyl bromide-induced OE lesions (Schwartz-Levy et al, 1991;Schwob et al, 1995).…”
Section: Increased Cell Death and Precursor Proliferation In ␤3gnt1supporting
confidence: 70%
“…Lesions in these non-neural systems also cause an increase in the overall rate of proliferation, which may be partly due to the aforementioned changes in cell cycle duration. Likewise, in the olfactory epithelium, the rate of proliferation of globose basal cells, expressed per unit length of epithelium, increases in response to lesions that destroy either the olfactory neurons alone or both neurons and nonneuronal cells (Schwartz Levey et al, 1991;Suzuki and Takeda, 1991;Can-and Farbman, 1992;Schwob et al, 1992Schwob et al, ,1995. Of course, mechanisms other than alteration of the mitotic cycle in olfactory and other epithelia are likely to impact on the proliferation rate.…”
Section: Discussionmentioning
confidence: 99%
“…For example, additional cells may be recruited into the mitotic cycle from GO and/or a greater proportion of daughter cells may re-enter the mitotic cycle after lesion and thereby expand the proliferating pool. Circumstantial evidence in support of the latter mechanism is observed after epithelial lesions produced by inhalation of methyl bromide gas (Schwob et al, 1995). Given that the olfactory epithelium is a self-renewing neuroepithelium easily accessible to manipulation and analysis, the search for mechanisms that regulate neurogenesis in the olfactory system is justified by the potentiality that the same mechanisms also regulate neurogenesis in the developing brain and spinal cord.…”
Section: Discussionmentioning
confidence: 99%
See 2 more Smart Citations