On the Life Span of Olfactory Receptor Neurons

Mackay‐Sim, Alan; Kittel, P. W.

doi:10.1111/j.1460-9568.1991.tb00081.x

Cited by 190 publications

(121 citation statements)

References 25 publications

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“…ORNs senesce throughout life, and are continually replaced from a population of precursor cells. These precursor cells are maintained at various stages of maturation, as identified by developmental markers (22,47). Thus, mature neurons that are lost through normal turnover or injury can be replaced rapidly by the terminal differentiation of immature neurons already in residence in the olfactory epithelium.…”

Section: Discussionmentioning

confidence: 99%

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Moon

Yoo

Matarazzo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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The discovery of stem cells in the adult central nervous system raises questions concerning the neurotrophic factors that regulate postnatal neuronal development. Olfactory receptor neurons (ORNs) are a useful model, because they are capable of robust neurogenesis throughout adulthood. We have investigated the role of leukemia inhibitory factor (LIF) in postnatal neuronal development by using ORNs as a model. LIF is a multifunctional cytokine implicated in various aspects of neuronal development, including phenotype determination, survival, and in response to nerve injury. LIF-deficient mice display significant increases, both in the absolute amount and in the number of cells expressing olfactory marker protein, a marker of mature ORNs. The maturation of ORNs was significantly inhibited by LIF in vitro. LIF activated the STAT3 pathway in ORNs, and transfection of ORNs with a dominant negative form of STAT3 abolished the effect of LIF. These findings demonstrate that LIF negatively regulates ORN maturation via the STAT3 pathway. Thus, LIF plays a critical role in controlling the transition of ORNs to maturity. Consequently, a population of ORNs is maintained in an immature state to facilitate the rapid repopulation of the olfactory epithelium with mature neurons during normal cell turnover or after injury.

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Section: Discussionmentioning

confidence: 99%

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Moon

Yoo

Matarazzo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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“…Soon after the cloning of odorant receptors, studies using radioactive in situ hybridization showed that these mRNAs are present in sensory axon terminals in the adult olfactory bulb (Ressler et al, 1994;Vassar et al, 1994). Because of the continuous neurogenesis that occurs in the adult olfactory epithelium (Mackay-Sim and Kittel, 1991), growing immature axons coexist with mature axons in the adult olfactory bulb. Given the low resolution of radioactive in situ hybridization, the maturity of the odorant receptor mRNA-containing axons could not be assessed.…”

Section: Introductionmentioning

confidence: 99%

Evidence for Developmentally Regulated Local Translation of Odorant Receptor mRNAs in the Axons of Olfactory Sensory Neurons

Dubacq¹,

Jamet²,

Trembleau³

2009

J. Neurosci.

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Odorant receptor mRNAs are transported within axons of olfactory sensory neurons that project into the olfactory bulb. Odorant receptor proteins have been identified along the distal part of these axons, which raises the possibility of their local synthesis in axons. We took advantage of the anatomical separation between the olfactory mucosa (which contains the sensory neuron cell bodies) and the bulb (which contains sensory axons but no sensory neuron cell bodies) to address this issue using a quantitative biochemical approach. Combining a method that separates polysome-associated mRNAs from untranslated mRNAs with a reverse transcription-quantitative PCR approach, we demonstrate that significant amounts of odorant receptor mRNAs are associated with polysomes in the sensory axons of the adult mouse bulb. We thus provide the first evidence for local synthesis of odorant receptor proteins in these axons. Interestingly, the rate of odorant receptor mRNA translation in axons is significantly greater during periods when the proportion of immature axons is higher (i.e., at postnatal day 4 or on regeneration after chemical lesion in adults). In contrast, the olfactory marker protein mRNA, which is restricted to mature axons, is translated at a low and constant level. Overall, we demonstrate that translation levels of odorant receptor mRNAs in axons are developmentally regulated, and positively correlated to the stage of axonal growth into the bulb. Given the established function of odorant receptors in the axonal wiring of sensory projections, we propose that this regulated axonal translation may play a role in the development and maintenance of the glomerular array.

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“…When olfactory neurons (ONs) die, new neurons are produced by division and differentiation of basal cells that reside in the olfactory epithelium [19,25,34], These newly formed neurons grow axons and are able to make the right synaptic connection with their target neurons in the olfactory bulb (OB) which is part of the central nervous system (CNS). The perrnis sivity of the adult OB to the growth ofaxons persists after transection of olfactory nerves [16,24] or lesioning of the olfactory nerve layer of the bulb [16].…”

Section: Introductionmentioning

confidence: 99%

Cultured olfactory ensheathing cells express nerve growth factor, brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor and their receptors

Woodhall

West

Chuah

2001

Molecular Brain Research

306

209

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In the primary olfactory pathway axons of olfactory neurons (ONs) are accompanied by ensheathing cells (ECs) as the fibres course towards the olfactory bulb. Ensheathing cells are thought to play an important role in promoting and guiding olfactory axons to their appropriate target. In recent years, studies have shown that transplants of ECs into lesions in the central nervous system (CNS) are able to stimulate the growth ofaxons and in some cases restore functional connections. In an attempt to identify a possible mechanism underlying EC support for olfactory nerve growth and CNS axonal regeneration, this study investigated the production of growth factors and expression of corresponding receptors by these cells. Three techniques immunohistochemistry, enzyme linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) were used to assess growth factor expression in cultured ECs. Immunohistochemistry showed that ECs expressed nerve growth factor (NGF), brain derived neurotrophic factor (BDNF) and glial cell-line derived neurotrophic factor (GDNF). ELISA confirmed the intracellular presence of NGF and BDNF and showed that, compared to BDNF, about seven times as much NGF was secreted by ECs. RT-PCR analysis demonstrated expression of mRNA for NGF, BDNF, GDNF and neurturin (NTN). In addition, ECs also expressed the receptors trkB, GFRa-1 and GFRa-2. The results of the experiments show that ECs express a number of growth factors and that BDNF in particular could act both in a paracrine and autocrine manner.

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On the Life Span of Olfactory Receptor Neurons

Cited by 190 publications

References 25 publications

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

Evidence for Developmentally Regulated Local Translation of Odorant Receptor mRNAs in the Axons of Olfactory Sensory Neurons

Cultured olfactory ensheathing cells express nerve growth factor, brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor and their receptors

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