2006
DOI: 10.4067/s0716-97602006000500002
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Role of nitric oxide during neurogenesis in the olfactory epithelium

Abstract: In mammals, neurogenesis continues during adulthood in restricted places of the nervous system, namely the subventricular zone, the dentate gyrus and the olfactory epithelium. A dual role of the second messenger nitric oxide has been reported in such places, either promoting or inhibiting proliferation of neuronal precursors depending on the cellular signal implicated. In this review the regulation of adult olfactory epithelium neurogenesis by nitric oxide is discussed.

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Cited by 10 publications
(7 citation statements)
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“…These proteins can inhibit neurogenesis in the OE at high concentrations and stimulate neurogenesis at low concentrations [29, 33]. Several other substances such as neurotrophins [34], pituitary adenylate cyclase‐activating polypeptide [35], dopamine [36], nitric oxide [37], insulin‐like growth factor 1 [38], brain‐derived neurotrophic factor, glial cell line‐derived neurotrophic factor, and ciliary neurotrophic factor [39] have also been suggested to influence differentiation of OE progenitors.…”
Section: Introductionmentioning
confidence: 99%
“…These proteins can inhibit neurogenesis in the OE at high concentrations and stimulate neurogenesis at low concentrations [29, 33]. Several other substances such as neurotrophins [34], pituitary adenylate cyclase‐activating polypeptide [35], dopamine [36], nitric oxide [37], insulin‐like growth factor 1 [38], brain‐derived neurotrophic factor, glial cell line‐derived neurotrophic factor, and ciliary neurotrophic factor [39] have also been suggested to influence differentiation of OE progenitors.…”
Section: Introductionmentioning
confidence: 99%
“…However, from the evidence that, irrespective of the etiology (inflammatory or noninflammatory), the nasal NO levels decrease in patients with decreased sense of smell ( 10 ), one can conclude that the lower nasal NO levels in patients with olfactory loss are more closely linked to the injury of olfactory sensory neurons rather than inflammation alone. Nonetheless, the recovery of smell loss is associated with the process of neurogenesis that involves an increase in the expression of inducible NOS in the basal progenerator cells secondary to the stimulation by leukemia inhibitory factor released from the injured neurons ( 11 ) ( Figure 1C ). The increase in nasal NO levels during the recovery phase from rhinitis-induced inflammation and anosmia is already well evident ( 2 ); I believe this can secondarily be due to the normalization of tryptophan catabolism.…”
mentioning
confidence: 99%
“…[15][16][17] Neurotrophic factors can act to enhance neuronal survival, regulate progenitor cell proliferation, and promote neurogenesis, lineage determination, neurotransmitter expression, and neuronal differentiation. 18 Recent studies have demonstrated that rat amniotic fluid mesenchymal stem cells may facilitate regeneration in the sciatic nerve after crush injury, and it may be due to the neurotrophic factors secreted by mesenchymal stem cells.…”
Section: Discussionmentioning
confidence: 99%