Transection of the olfactory nerves induces expression of nerve growth factor receptor in mouse olfactory epithelium

Miwa, Takaki; Moriizumi, Tetsuji; Sakashita, Hideo; Kimura, Yasuyuki; Donjo, Takeo; Furukawa, Mitsuru

doi:10.1016/0304-3940(93)90681-a

Cited by 27 publications

(9 citation statements)

References 12 publications

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“…And the amount of ORNs (basal cells, immature neurons and mature neurons) in CUMS rats were decreased, as demonstrated by A c c e p t e d M a n u s c r i p t immunohistochemistry for p75NGFR, GAP43 and OMP, respectively. P75NGFR is expressed in basal cells and play a significant role in regeneration of ORNs [26]. GAP43 is a neuronal molecule expressed by immature ORNs [27,28].…”

Section: Discussionmentioning

confidence: 99%

Reduced amount of olfactory receptor neurons in the rat model of depression

Yang

Wang

et al. 2015

Neuroscience Letters

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Section: Discussionmentioning

confidence: 99%

Reduced amount of olfactory receptor neurons in the rat model of depression

Yang

Wang

et al. 2015

Neuroscience Letters

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“…These factors include brain‐derived neurotrophic factor (BDNF; Buckland and Cunningham, 1999), glial‐derived neurotrophic factor (GDNF; Buckland and Cunningham, 1999), fibroblast growth factor‐2 (FGF2; Goldstein et al, 1997), insulin growth factor‐1 (IGF1; Federico et al, 1999), transforming growth factor‐β (TGFβ; Farbman and Bucholz, 1996), and leukemia inhibitory factor (LIF; Satoh and Yoshida, 1997). In addition, other proteins, such as nerve growth factor (NGF), may be transported retrogradely to the olfactory epithelium from the olfactory bulb (Miwa et al, 1993), although it is unclear whether NGF is normally expressed in nonbulbectomized epithelium (Aiba et al, 1993; Roskams et al, 1996). Detailed functional and mechanistic data utilizing these proteins both in vitro and in vivo, however, are lacking.…”

Section: Olfactory Epithelium Structure and Functionmentioning

confidence: 99%

Regulation of olfactory neurogenesis by amidated neuropeptides

Hansel

Eipper

Ronnett

2001

J of Neuroscience Research

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The existence of stem cells in the CNS raises issues concerning the ability of nervous tissues to regenerate in the adult mammal and provides new perspectives on the treatment of degenerative disease and traumatic injury of the nervous system. These cells have a relatively limited range of locations within the nervous system and include cells of the rostral migratory stream, hippocampus, retina, and olfactory epithelium. The olfactory epithelium has been studied as a model of adult neuronal regeneration, with neuronal precursor/basal cells serving as the olfactory "stem cells." The identification of factors that promote neuronal proliferation or regeneration within the olfactory epithelium can provide clues to the process of adult mammalian nervous system repair and treatment. Multiple factors have been examined that appear to influence the proliferation and subsequent maturation of basal cells. These factors include nerve growth factor, fibroblast growth factor-2, epidermal growth factor, and insulin/insulin-like growth factor-1. Recently, two amidated neuropeptides, neuropeptide Y (NPY) and pituitary adenylate cyclase-activating polypeptide (PACAP38), identified in the olfactory epithelium have been shown to promote dramatically neuronal proliferation. The effects of NPY and PACAP suggest that amidated neuropeptides may serve a broad developmental and regenerative role in the mammalian olfactory epithelium.

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“…Qin-Wei et al (1994) reported that NGF rescues embryonic chick motoneurons from deafferentation-induced cell death, although NGF does not rescue the same neurons from programmed cell death (Oppenheim et al, 1988) . Injury, including that associated with cell dissociation and culture, has been shown to induce the expression of both high-and low-affinity NGF receptors in several different systems (Pioro and Cuello, 1990;Cheng and Mattson, 1991 ;Miwa et al, 1993) . Neurons in embryonic hippocampal and cortical cultures express high levels of p75, the low-affinity NGF receptor (Cheng and Mattson, 1991 ;Mattson et al, 1993d) .…”

Section: Trophic Factors and Radicals In Hippocampal Neuronsmentioning

confidence: 99%

Neurotrophic Factors Attenuate Glutamate‐Induced Accumulation of Peroxides, Elevation of Intracellular Ca²⁺ Concentration, and Neurotoxicity and Increase Antioxidant Enzyme Activities in Hippocampal Neurons

Mattson

Lovell²,

Furukawa³

et al. 1995

Journal of Neurochemistry

611

281

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Exposure of cultured rat hippocampal neurons to glutamate resulted in accumulation of cellular peroxides (measured using the dye 2,7‐dichlorofluorescein). Peroxide accumulation was prevented by an N‐methyl‐d‐aspartate (NMDA) receptor antagonist and by removal of extracellular Ca2+, indicating the involvement of NMDA receptor‐induced Ca2+ influx in peroxide accumulation. Glutamate‐induced reactive oxygen species contributed to loss of Ca2+ homeostasis and excitotoxic injury because antioxidants (vitamin E, propyl gallate, and N‐tert‐butyl‐α‐phenylnitrone) suppressed glutamate‐induced elevation of intracellular Ca2+ concentration ([Ca2+]i) and cell death. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and brain‐derived neurotrophic factor (BDNF), but not ciliary neurotrophic factor, each suppressed accumulation of peroxides induced by glutamate and protected neurons against excitotoxicity. bFGF, NGF, and BDNF each increased (to varying degrees) activity levels of superoxide dismutases and glutathione reductase. NGF increased catalase activity, and BDNF increased glutathione peroxidase activity. The ability of the neurotrophic factors to suppress glutamate toxicity and glutamate‐induced peroxide accumulation was attenuated by the tyrosine kinase inhibitor genistein, indicating the requirement for tyrosine phosphorylation in the neuroprotective signal transduction mechanism. The data suggest that glutamate toxicity involves peroxide production, which contributes to loss of Ca2+ homeostasis, and that induction of antioxidant defense systems is a mechanism underlying the [Ca2+]i‐stabilizing and excitoprotective actions of neurotrophic factors.

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Transection of the olfactory nerves induces expression of nerve growth factor receptor in mouse olfactory epithelium

Cited by 27 publications

References 12 publications

Reduced amount of olfactory receptor neurons in the rat model of depression

Reduced amount of olfactory receptor neurons in the rat model of depression

Regulation of olfactory neurogenesis by amidated neuropeptides

Neurotrophic Factors Attenuate Glutamate‐Induced Accumulation of Peroxides, Elevation of Intracellular Ca²⁺ Concentration, and Neurotoxicity and Increase Antioxidant Enzyme Activities in Hippocampal Neurons

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Transection of the olfactory nerves induces expression of nerve growth factor receptor in mouse olfactory epithelium

Cited by 27 publications

References 12 publications

Reduced amount of olfactory receptor neurons in the rat model of depression

Reduced amount of olfactory receptor neurons in the rat model of depression

Regulation of olfactory neurogenesis by amidated neuropeptides

Neurotrophic Factors Attenuate Glutamate‐Induced Accumulation of Peroxides, Elevation of Intracellular Ca2+ Concentration, and Neurotoxicity and Increase Antioxidant Enzyme Activities in Hippocampal Neurons

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Neurotrophic Factors Attenuate Glutamate‐Induced Accumulation of Peroxides, Elevation of Intracellular Ca²⁺ Concentration, and Neurotoxicity and Increase Antioxidant Enzyme Activities in Hippocampal Neurons