Effects of various causes, such as aging, smoking, and epithelial damage, on the global gene expression profiles of the mouse nasal mucosa and olfactory bulb
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE150694 | GEO | 2020/05/28
REPOSITORIES: GEO
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Project description:The olfactory system is a part of the mammalian central nervous system and is characterized by neurogenesis and replacement of degenerated neurons. Clinically, it has been reported that the elderly has a high incidence of olfactory impairment. However, the molecular mechanisms underlying aging-associated defect of olfaction have yet been unclear. To elucidate this problem, we performed micoarray analysis against murine olfactory epithelium and compared the transcriptome of them between young-adult and aged mice.
2018-05-11 | GSE103191 | GEO
Project description:The olfactory bulb (OB) is a critical component of mammalian olfactory neuroanatomy. Beyond being the first and sole relay station for olfactory information to the rest of the brain, it also contains elaborate stereotypical circuitry that is considered essential for olfaction. Indeed, substantial lesions of the OB in rodents lead to anosmia. Here, we examined the circuitry that underlies olfaction in a mouse model with severe developmental degeneration of the OB. These mice could perform odor-guided tasks and even responded normally to innate olfactory cues. Despite the near total loss of the OB, piriform cortex in these mice responded to odors normally and its neural activity sufficed to decode odor identity. We found that sensory neurons expressthe full repertoire of olfactory receptors and their axons project primarily to the rudiments of the OB, but also ectopically, to olfactory cortical regions. Within the OB, the number of principal neurons was greatly reduced and the morphology of their dendrites was abnormal, extending over large regions within the OB. Glomerular organization was totally lost in the severe cases of OB degeneration and altered in the more conserved OBs, and the transcriptional profile of the glomerular layer was highly inflammatory. This study shows that olfactory functionality can be preserved despite reduced and aberrant circuitry that is missing many of the elements that are believed to be essential for olfaction, and may explain reported retention of olfaction in humans with degenerated OBs
2023-09-04 | GSE241951 | GEO
Project description:Olfactory sensory neurons distinguish a large variety of odor molecules and direct the information through their axons to the olfactory bulb, the first site for the processing of olfactory information in the brain. Olfaction is very important for most mammals for the maintenance of a good quality of life. Accumulating evidences endorse that olfactory sensory decline is connected with neurodegenerative disorders including schizophrenia, depression, multiple sclerosis, Huntington's, Alzheimer's and Parkinson's diseases. For several decades, neuroanatomical, volumetric, and histological approaches have been the gold standard techniques employed to characterize the olfactory bulb functionality. Diagnosis and treatment of olfactory dysfunction remain significant health care challenges to society. Novel strategies and clues that assist in the identification of biomarker and drug development for aid in the prevention and cure of neurological diseases are necessary. However, little attention has been focused specifically on the molecular composition of the olfactory bulb from the perspective of proteomics. To this end, an in-depth mapping of the olfactory bulb proteome was carried out using high resolution tandem mass spectrometry, revealing a repertoire of 7,754 proteins. A large proportion of the identified proteins were predicted to be involved in diverse biological processes including signal transduction, metabolism, transport, olfaction and protein synthesis. Pathway analysis of the identified proteins shows that, these proteins are predominantly involved in metabolic and neural processes, chromatin modeling, and synaptic vesicle transport associated with neuronal transmission. In total, our study offers valuable understandings into the molecular composition of the human olfactory bulb proteome that could possibly help neuroscience community to understand the olfactory bulb better and open avenues for intervention strategies for olfactory dysfunction in the future.
2017-08-23 | PXD005629 | Pride
Project description:To investigate the repertoire of olfactory receptors when the olfactory bulb is 30- 10% of normal size. Olfactory bulb was degenerated due conditional transgenic expression of the VEGF blocker sFlt1 in the brain at embryonic day 13.5
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Project description:Nasal mucosa and olfactory bulb are separated by the cribriform plate which is perforated by olfactory nerves. We have previously demonstrated that the cribriform plate is permissive for T cells and monocytes and that viruses can enter the bulb upon intranasal injection by axonal transportation. Therefore, we hypothesized that nasal mucosa and olfactory bulb are equipped to deal with constant infectious threats. To detect genes involved in this process, we compared gene expression in nasal mucosa and bulb of mice kept under specific pathogen free (SPF) conditions to gene expression of mice kept on non-SPF conditions using RNA deep sequencing. We found massive alterations in the expression of immune-related genes of the nasal mucosa, while the bulb did not respond immunologically. The absence of induction of immune-related genes in the olfactory bulb suggests effective defence mechanisms hindering entrance of environmental pathogens beyond the outer arachnoid layer. The genes detected in this study may include candidates conferring susceptibility to meningitis.
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Project description:Using the highly sensitive miRNA array, we screened 40 microRNAs abundant in the olfactory bulb and we explored the functions of these miRNAs in the olfactory bulb by Gene Ontology and Kyoto Encyclopedia of Genes annotation. The enrichment results indicated that these miRNAs mainly participated in the axon guidance process. Furthermore, the quantitative real-time polymerase chain reaction, immunohistochemistry, and dual luciferase reporter assay results showed that miR-30c is a specific regulator of semaphorin-3A, which will give new insights in disclosing the mechanism of functional maintenance and sexual-specific differentiation of the olfactory bulb. In this study, three samples from steady-state mice were used to acquire the miRNA expression profiling and the function of the abudant miRNAs in the olfactory bulb were analyzed by bioinformatic methods.Finally, miR-30c was experimentally validated to be a regulator of semaphorin-3A, an important axon guidance cue in the nervous system.
2014-08-27 | E-GEOD-55463 | biostudies-arrayexpress
Project description:The aim of this study was to use global gene expression profiling to define intrinsic molecular differences that distinguish olfactory ensheathing cells from mucosa (OM-OECs) from olfactory ensheathing cells from olfactory bulb (OB-OECs). 10,000 OECs from olfactory mucosa (OM) or olfactory bulb (OB) were isolated from 4 rats.
2009-12-02 | GSE19250 | GEO
Project description:During embryonic development, the olfactory placode (OP) gives rise to various populations of neurons; these include putative olfactory pioneer neurons, different neurons of unknown identity and function, cells of the terminal nerve, and the Gonadotropin-releasing hormone-1 (GnRH-1) neurons. In mice, the GnRH-1 neurons are first detectable in the developing olfactory system around mid-gestation. From here, the GnRH-1 neurons migrate, along the axons of the terminal nerve (TN), to various regions of the developing brain. Once in the brain, the GnRH-1 neurons play a central role in controlling the hypothalamic-pituitary-gonadal (HPG) axis. Early migratory neurons forming from the olfactory placode have been proposed to play a vital role in inducing olfactory bulb morphogenesis. Kallmann syndrome is a condition characterized by defective development of the olfactory system and infertility. Murine studies have demonstrated the critical role of the Prokineticin 2-Prokinteicin Receptor 2 pathway in olfactory bulb morphogenesis and GnRH-1 neuronal migration. Loss-of-function Prokr2 mutations cause both Kallmann syndrome associated with bulb agenesis and normosmic idiopathic hypogonadotropic hypogonadism (nIHH). Following Prokr2 expression and lineage tracing, we found that Prokr2 is not expressed by the cells of the developing olfactory bulb but by migratory putative pioneer/terminal nerve neurons. Performing single-cell-RNA-sequencing, we identified genes enriched in the migratory cells of the putative terminal nerve. By integrating genetic lineage tracing and single-cell transcriptomics, we identified previously undescribed populations of migratory neurons that appear to be enriched in the expression of several genes related to olfactory defects, GnRH migratory deficiencies and infertility.
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Project description:There is an emerging concern that particulate air pollution increases the risk of cranial nerve disease onset. Small nanoparticles, mainly derived from diesel exhaust particles reach the olfactory bulb by their nasal depositions. It has been reported that diesel exhaust inhalation causes inflammation of the olfactory bulb and other brain regions. However, these toxicological studies have not evaluated animal rearing environment. We hypothesized that rearing environment can change mice phenotypes and thus might alter toxicological study results. In this study, we exposed mice to diesel exhaust inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days after rearing in a standard cage or environmental enrichment conditions. Microarray analysis found that expression levels of 112 genes were changed by diesel exhaust inhalation. Functional analysis using Gene Ontology revealed that the dysregulated genes were involved in inflammation and immune response. This result was supported by pathway analysis. Quantitative RT-PCR analysis confirmed 10 genes. Interestingly, background gene expression of the olfactory bulb of mice reared in a standard cage environment was changed by diesel exhaust inhalation, whereas there was no significant effect of diesel exhaust exposure on gene expression levels of mice reared with environmental enrichment. The results indicate for the first time that the effect of diesel exhaust exposure on gene expression of the olfactory bulb was influenced by rearing environment. Rearing environment, such as environmental enrichment, may be an important contributive factor to causation in evaluating still undefined toxic environmental substances such as diesel exhaust. RNA sample was taken from olfactory bulb of 56-day-old mouse received diesel exhaust (DE) inhalation at 90 micro g/m3, 8 hours/day, for 28 consecutive days, while control RNA was taken from mouse received clean air, after rearing in a standard cage or environmental enrichment conditions. Comparisons among groups were made by one-color method with normalized data from Cy3 channels for data analysis.
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Project description:Proteome analysis of mouse brain tissue samples from olfactory bulb of middle-aged (8-13 months) female mice.
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