Age-related changes in microvillar cells of rat olfactory epithelium

Kwon, Bum Sun; Kim, Min Kyu; Kim, Woo Ho; Pyo, Jae Sung; Cheon, Young Hee; Ik, Choong; Nam, Sang Yong; Baik, Tai-Kyoung; Lee, Byung Lan

doi:10.1016/j.neulet.2004.11.094

Cited by 11 publications

(6 citation statements)

References 16 publications

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“…3E). These might represent the nonneuronal cell type "1A6' ' (Carr et al, 1991;Kwon et al, 2005). The microvillar-like NSE-positive cells do not represent the "fourth type'' of cell (Moran et al, 1982b) within the OE, which is thought to be a chemoreceptor cell (Moran et al, 1982a;.…”

Section: Nse Expression In Non-neuronal Cellsmentioning

confidence: 99%

Olfactory epithelia differentially express neuronal markers

Weiler

Benali

2005

J Neurocytol

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All three olfactory epithelia, the olfactory epithelium proper (OE), the septal organ of Masera (SO), and the vomeronasal organ of Jacobson (VNO) originate from the olfactory placode. Here, their diverse neurochemical phenotypes were analyzed using the immunohistochemical expression pattern of different neuronal markers. The olfactory bulb (OB) served as neuronal control. Neuronal Nuclei Marker (NeuN) is neither expressed in sensory neurons in any of the three olfactory epithelia, nor in relay neurons (mitral/tufted cells) of the OB. However, OB interneurons (periglomerular/granule cells) labeled, as did supranuclear structures of VNO supporting cells and VNO glands. Protein Gene Product 9.5 (PGP9.5 = C-terminal ubiquitin hydrolase L1 = UCHL1) expression is exactly the opposite: all olfactory sensory neurons express PGP9.5 as do OB mitral/tufted cells but not interneurons. Neuron Specific Enolase (NSE) expression is highest in the most apically located OE and SO sensory neurons and patchy in VNO. In contrast, the cytoplasm of the most basally located neurons of OE and SO immunoreacted for Growth Associated Protein 43 (GAP-43/B50). In VNO neurons GAP-43 labeling is also nuclear. In the cytoplasm, Olfactory Marker Protein (OMP) is most intensely expressed in SO, followed by OE and least in VNO neurons; further, OMP is also expressed in the nucleus of basally located VNO neurons. OB mitral/tufted cells express OMP at low levels. Neurons closer to respiratory epithelium often expressed a higher level of neuronal markers, suggesting a role of those markers for neuronal protection against take-over. Within the VNO the neurons show clear apical-basal expression diversity, as they do for factors of the signal transduction cascade. Overall, expression patterns of the investigated neuronal markers suggest that OE and SO are more similar to each other than to VNO.

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Section: Nse Expression In Non-neuronal Cellsmentioning

confidence: 99%

Olfactory epithelia differentially express neuronal markers

Weiler

Benali

2005

J Neurocytol

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“…It is possible that sustentacular cells perform a dual role as both microglia and astroglia, but a marker of microglia, OX-42, did not change with age (Weiler and Farbman, 1998 ; Kim et al, 2005 ). The number and appearance of microvillar cells, a somewhat recently discovered cell type in the OE whose function is as of yet unclear, is also altered with aging (Kwon et al, 2005 ). Additionally, the rate of spontaneous lesions of the olfactory epithelium increases with age, suggesting an age-related dysfunction leading to pathogenesis (Kondo et al, 2009 ).…”

Section: Introductionmentioning

confidence: 99%

Injury in aged animals robustly activates quiescent olfactory neural stem cells

Brann

Ellis

et al. 2015

Front. Neurosci.

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While the capacity of the olfactory epithelium (OE) to generate sensory neurons continues into middle age in mice, it is presumed that this regenerative potential is present throughout all developmental stages. However, little experimental evidence exists to support the idea that this regenerative capacity remains in late adulthood, and questions about the functionality of neurons born at these late stages remain unanswered. Here, we extend our previous work in the VNO to investigate basal rates of proliferation in the OE, as well as after olfactory bulbectomy (OBX), a commonly used surgical lesion. In addition, we show that the neural stem cell retains its capacity to generate mature olfactory sensory neurons in aged animals. Finally, we demonstrate that regardless of age, a stem cell in the OE, the horizontal basal cell (HBC), exhibits a morphological switch from a flattened, quiescent phenotype to a pyramidal, proliferative phenotype following chemical lesion in aged animals. These findings provide new insights into determining whether an HBC is active or quiescent based on a structural feature as opposed to a biochemical one. More importantly, it suggests that neural stem cells in aged mice are responsive to the same signals triggering proliferation as those observed in young mice.

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“…The IP3R3 + microvillous cells are resistant to bulbectomy-induced neuronal apoptosis (Jia et al, 2013), and are likely derived from olfactory stem cell proliferation and differentiation, and have a slow turnover rate (Pfister et al, 2012). A previous study reported that aged rat OE microvillous cells morphologically similar to IP3R3 + microvillous cells had marked hypertrophy but were resistant to age-related reductions in cell number compared to other OE cell types (Kwon et al, 2005). In the present study, using a transgenic IP3R3-tauGFP mouse we found age-dependent reductions in IP3R3 + cells and NPY + cells but seldom observed hypertrophy of IP3R3 + microvillous cells in aged mouse OE.…”

Section: Discussionmentioning

confidence: 98%

Effect of IP3R3 and NPY on age-related declines in olfactory stem cell proliferation

Jia

Hegg

2015

Neurobiology of Aging

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Losing the sense of smell due to aging compromises health and quality of life. In the mouse olfactory epithelium (OE) aging reduces the capacity for tissue homeostasis and regeneration. The microvillous cell subtype that expresses both inositol trisphosphate receptor type 3 (IP3R3) and the neuroproliferative factor neuropeptide Y (NPY) is critical for regulation of homeostasis, yet its role in aging is undefined. We hypothesized that an age-related decline in IP3R3 expression and NPY signaling underlie age-related homeostatic changes and olfactory dysfunction. We found a decrease in IP3R3+ and NPY+ microvillous cell numbers and NPY protein, and a reduced sensitivity to NPY-mediated proliferation over 24 months. However, in IP3R3-deficient mice, there was no further age-related reduction in cell numbers, proliferation, or olfactory function compared to wild-type. The proliferative response was impaired in aged IP3R3-deficient mice when injury was caused by satratoxin-G, which induces IP3R3-mediated NPY release, but not by bulbectomy, which does not evoke NPY release. These data identify IP3R3 and NPY signaling as targets for improving recovery following olfactotoxicant exposure.

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Age-related changes in microvillar cells of rat olfactory epithelium

Cited by 11 publications

References 16 publications

Olfactory epithelia differentially express neuronal markers

Olfactory epithelia differentially express neuronal markers

Injury in aged animals robustly activates quiescent olfactory neural stem cells

Effect of IP3R3 and NPY on age-related declines in olfactory stem cell proliferation

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