BDNF expression in olfactory bulb and epithelium during regeneration of olfactory epithelium
ABSTRACT To further understand the roles of growth factors in the olfactory neurogenesis, we studied the mRNA levels of diverse genes in olfactory bulb (OB) and olfactory epithelium (OE) during the regeneration process of OE. mRNA expression levels of various genes in the OB and OE during the regeneration processes of OE from damage induced by methimazole administration were studied by DNA microarray analysis. The results were confirmed by quantitative real-time RT-PCR and immunohistochemistry. Expression levels of various genes dramatically changed during the observation period. Among them, mRNA expression of BDNF dramatically increased in OE during the first 7 days and then decreased. In contrast, mRNA expression of BDNF in OB significantly decreased during the first 7 days after administration and then gradually increased. The changes in the mRNA levels of OMP in OB precisely followed those of OMP in OE and OB. The present results suggest that BDNF in OE contributes to the early stage of regeneration, and BDNF in OB has its role in the late stage of regeneration of olfactory receptor neurons (ORNs).
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- "In the olfactory system, BDNF has been implicated in the generation and differentiation of ORNs as well as the regulation of branching of ORN axons in their target glomeruli in the OB (Calof et al., 1998; Clevenger et al., 2008). In addition, several studies have documented that the neurotrophins NGF and BDNF sequentially promote proliferation of the developing olfactory neuronal precursors (Clevenger et al., 2008; Newman et al., 2000; Uranagase et al., 2012). Both NGF and BDNF increase the expression of cyclin D1 and cyclin-dependent kinase 4 (cdk4) affecting the proliferation kinetics of the ORN precursors (Simpson et al., 2007). "
ABSTRACT: 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. Copyright © 2014 Elsevier GmbH. All rights reserved.Annals of Anatomy - Anatomischer Anzeiger 11/2014; 198. DOI:10.1016/j.aanat.2014.10.010 · 2.08 Impact Factor
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ABSTRACT: Brain- derived neurotrophic factor (BDNF) is linked to neurodegenerative diseases (e.g. Alzheimer disease and Parkinson disease) which are often characterized by olfactory impairment. A specific single nucleotide polymorphism of the BDNF gene, the Val66Met, modulates intracellular trafficking and activity-dependent secretion of BDNF protein. The aim of this study was to investigate a possible association between brain- derived neurotrophic factor Val66Met polymorphism and olfactory function, a well-known biomarker for neurodegeneration, in healthy young adults. A total of 101 subjects (45 males, age 38.7 +/- 9.4 years) were assessed using the Sniffin' Sticks Extended Test, a highly reliable commercial olfactory test composed of three sub-parts, calculating olfactory threshold (sensitivity), odor discrimination and odor identification. The Val66Met polymorphism was determined by polymerase chain reaction -restriction fragment length polymorphism (PCR-RFLP) analysis. An impaired function in Met carriers was found, especially when compared to subjects with Val/Val genotype, in the threshold (5.5 +/- 2.0 vs 6.5 +/- 1.8, p = 0.009), discrimination (10.3+/- 2.5 vs 11.9 +/- 2.2, p = 0.002), and identification task (13.3 +/- 1.6 vs 14.1 +/- 1.3, p = 0.007), as well as in the overall TDI Score (29.1 +/- 4.5 vs 32.6 +/- 3.9, p < 0.001). These findings appear to have implications for the evaluation of olfactory function and the relation of its impairment to cognitive decline and neurodegenerative disease.Journal of Biomedical Science 08/2013; 20(1):57. DOI:10.1186/1423-0127-20-57 · 2.74 Impact Factor
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ABSTRACT: BDNF (Brain Derived Neurotrophic Factor) is a member of the neurotrophin family, and it is implicated in regulating brain development and function. The BDNF gene organization and coding sequence are conserved in all vertebrates.. The present survey was conducted in a teleost fish, Nothobranchius furzeri, because it is an emerging model of ageing studies due to its short lifespan and shows the high rate of adult neurogenesis typical of anamniotes. The present survey reports: a) the identification and characterization of the cDNA fragment encoding BDNF protein; b) the localization of BDNF in the whole brain. BDNF mRNA expression was assessed by in situ hybridization, by employing antisense RNA probe; BDNF protein was detected by employing a sensitive immunohistochemical technique, along with highly specific affinity-purified antibodies to BDNF. Both BDNF mRNA and protein were detected in neurons and glial cells of all regions of the brain of N. furzeri. Interestingly, BDNF was localized also in brain areas involved in adult neurogenic activities, suggesting a specific role for this neurotrophic factor in controlling cell proliferation. These results provide baseline information for future studies concerning BDNF involvement in ageing processes of the teleost brain. J. Comp. Neurol., 2013. © 2013 Wiley Periodicals, Inc.The Journal of Comparative Neurology 04/2014; 522(5). DOI:10.1002/cne.23457 · 3.51 Impact Factor