RESUMO
Olfactory epithelium has the capability to continuously regenerate olfactory receptor neurons throughout life. Adult neurogenesis results from proliferation and differentiation of neural stem cells, and consequently, olfactory neuroepithelium offers an excellent opportunity to study neural regeneration and the factors involved in the maintenance and regeneration of all their cell types. We analyzed the expression of BDNF in the olfactory system under normal physiological conditions as well as during a massive regeneration induced by chemical destruction of the olfactory epithelium in Xenopus laevis larvae. We described the expression and presence of BDNF in the olfactory epithelium and bulb. In normal physiological conditions, sustentacular (glial) cells and a few scattered basal (stem) cells express BDNF in the olfactory epithelium as well as the granular cells in the olfactory bulb. Moreover, during massive regeneration, we demonstrated a drastic increase in basal cells expressing BDNF as well as an increase in BDNF in the olfactory bulb and nerve. Together these results suggest an important role of BDNF in the maintenance and regeneration of the olfactory system.
Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Bulbo Olfatório/patologia , Bulbo Olfatório/fisiopatologia , Mucosa Olfatória/patologia , Mucosa Olfatória/fisiopatologia , Animais , Regeneração Nervosa/fisiologia , Neurogênese/fisiologia , Xenopus laevisRESUMO
INTRODUCTION: Olfactory neuroepithelium (ON) biopsy has several therapeutic applications for both disorders of olfaction and neurodegenerative diseases. Successful collection of ON is still anything but routine due to a dearth of studies on the distribution of ON in the superior and middle turbinates. AIM: To determine the location in which ON is most likely to be present in endoscopically removed cadaver superior and middle turbinates as well as the influences of gender, age, and naris side on the presence of ON and the extent to which it is present. METHODS: We conducted a prospective anatomical study. The superior and middle turbinates on both sides endoscopically removed from 25 fresh cadavers (less than 12 h post-mortem). The turbinates were halved into anterior and posterior segments for a total of 200 specimens, which were analyzed after hematoxylin and eosin and immunohistochemical staining. Hematoxylin and eosin-stained slides were subjected to blind examination by 3 independent pathologists, and the presence of ON was graded on a 5-point scale from 0 to 4. Kappa measurement was used to determine the agreement between pairs of observers. RESULTS: ON was present in 82.9% of superior turbinate samples and in 17.1% of middle turbinate samples. Immunohistochemistry detected ON in superior turbinates only by S-100 staining and only in 15 fragments. Gender, age, and naris side had no statistically significant effects on the presence of ON. CONCLUSION: When biopsying ON, the posterior portion of the superior turbinate should be targeted whenever possible because it has the highest concentration of ON among the nasal structures.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso de 80 Anos ou mais , Biópsia , Mucosa Olfatória/fisiopatologia , Conchas Nasais , Cadáver , Corantes , Transtornos do OlfatoRESUMO
Alzheimer's disease (AD) is considered to be the number one health problem and seems to be reaching epidemic proportion in the USA. The cause of AD is not known, a reliable animal model of the disease has not been found and appropriate treatment of this dementia is wanting. The present review focuses on the possibility that a virus or exogenous toxic materials may gain access to the CNS using the olfactory mucosa as a portal of entry. Anterograde and retrograde transport of the virus/zeolites to olfactory forebrain regions, which receive primary and secondary projections from the main olfactory bulb (MOB) and which, in turn, project centrifugal axons to the MOB, may initiate cell degeneration at such loci. Pathological changes may, thus, be initially confined to projecting and intrinsic neurons localized in cortical and subcortical olfactory structures; arguments are advanced which favor the view that excitotoxic phenomena could be mainly responsible for the overall degenerative picture. Neurotoxic activity may follow infection by the virus itself, be facilitated by loss of GABAergic terminals in olfactory cortex, develop following repeated episodes of physiological long term potentiation (which unmasks NMDA receptors) or be due to excessive release, faculty re-uptake or altered glutamate receptor sensitivity. Furthermore, a reduction in central inhibitory inputs to the MOB might then result in disinhibition of mitral/tufted neurons and enhance the excitotoxic phenomena in the MOB projecting field. Within this context, and in line with recent studies, it is believed that pathology begins at cortical (mainly olfactory) regions, basal forebrain neurons being secondarily affected due to retrograde degeneration. In addition, failure to produce a critical level of neurotrophic factors by a damaged MOB and olfactory cortex, could adversely affect survival of basal cholinergic neurons which innervate both regions. Support for these hypothesis is provided, first, by recent reports on pathological findings in AD brains which seem to involve preferentially the olfactory and entorhinal cortices, the olfactory amygdala and the hippocampus, all of which receive primary or secondary projections from the MOB; secondly, by the presence of severe olfactory deficits in the early stages of the disease, mainly of a discriminatory nature, which points to a malfunction of central olfactory structures.