Signaling pathways and survival effects of BDNF and NT-3 on cultured cerebellar granule cells

Nonomura, Takeshi; Kubo, Takekazu; Oka, Tetsushi; Shimoke, Koji; Yamada, Masashi; Enokido, Yasushi; Hatanaka, Hiroshi

doi:10.1016/s0165-3806(96)00130-7

Cited by 92 publications

(86 citation statements)

References 36 publications

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“…1, B and C). This is in accord with results obtained in survival assays and should be viewed alongside evidence that the neurons do not express functional levels of TrkA or TrkC receptors (32). The B ANT peptide inhibits the NT-4 response in a dose-dependent manner, with a full inhibition seen at ϳ125 M (Fig.…”

Section: Resultssupporting

confidence: 89%

Overcoming the Inhibitors of Myelin with a Novel Neurotrophin Strategy

Williams

Maison

et al. 2005

Journal of Biological Chemistry

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Section: Resultssupporting

confidence: 89%

Overcoming the Inhibitors of Myelin with a Novel Neurotrophin Strategy

Williams

Maison

et al. 2005

Journal of Biological Chemistry

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“…12) whereas NGF had no effect on either cell survival or neurite outgrowth. This is in accordance with other published data (Courtney et al, 1997;Nonomura et al, 1996), and our own quantitative RT-PCR results indicating very low expression of the NGF receptor, TrkA in the CGNs (not shown). Thus, the high-content assay was able to reveal expected effects of known neurotrophins validating the assay setup.…”

Section: Hcs In Small-scale Analysissupporting

confidence: 94%

Image-Based High-Content Screening in Drug Discovery

Götte¹,

Gabriel²

2011

Drug Discovery and Development - Present and Future

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“…Therefore, we demonstrate that PI 3-kinase pathway seems to mediate the survival-promoting effects induced by this family of neurotrophic factors. The role of the PI 3-kinase pathway as a mediator of the trophic effects of several trophic factors has been described previously in BDNF-mediated survival of cultured cerebellar granule neurons (Nonomura et al, 1996;Shimoke et al, 1997) or spinal cord MTNs (Dolcet et al, 1999), in NGF maintained PC12 or SGC cells (Yao and Cooper, 1995;Crowder and Freeman, 1998), and in cerebellar granule neurons maintained with IGF-1 (D' Mello et al, 1997;Dudek et al, 1997;Miller et al, 1997). However, the present work is the first demonstration of the involvement of the PI 3-kinase pathway in mediating the survival-promoting effects of the GDN F family of neurotrophic factors.…”

Section: Discussionmentioning

confidence: 77%

Receptors of the Glial Cell Line-Derived Neurotrophic Factor Family of Neurotrophic Factors Signal Cell Survival through the Phosphatidylinositol 3-Kinase Pathway in Spinal Cord Motoneurons

et al. 1999

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The members of the glial cell line-derived neurotrophic factor (GDNF) family of neurotrophic factors (GDNF, neurturin, persephin, and artemin) are able to promote in vivo and in vitro survival of different neuronal populations, including spinal cord motoneurons. These factors signal via multicomponent receptors that consist of the Ret receptor tyrosine kinase plus a member of the GDNF family receptor ␣ (GRF␣) family of glycosylphosphatidylinositol-linked coreceptors. Activation of the receptor induces Ret phosphorylation that leads the survival-promoting effects. Ret phosphorylation causes the activation of several intracellular pathways, but the biological effects caused by the activation of each of these pathways are still unknown. In the present work, we describe the ability of the GDNF family members to promote chicken motoneuron survival in culture. We show the presence of Ret and GFR␣-1, GFR␣-2, and GFR␣-4 in chicken motoneurons using in situ hybridization and reverse transcription-PCR techniques. By Western blot analysis and kinase assays, we demonstrate the ability of these factors to induce the phosphatidylinositol 3 kinase (PI 3-kinase) and the extracellular regulated kinase (ERK)-mitogen-activated protein (MAP) kinase pathways activation. To characterize the involvement of these pathways in the survival effect, we used the PI 3-kinase inhibitor LY 294002 and the MAP kinase and ERK kinase (MEK) inhibitor PD 98059. We demonstrate that LY 294002, but not PD 98059, prevents GDNF-, neurturin-, and persephin-induced motoneuron survival, suggesting that PI 3-kinase intracellular pathway is responsible in mediating the neurotrophic effect. Key words: GDNF; persephin; neurturin; artemin; motoneuron; neurotrophic factor; GFR␣ receptors; chicken; intracellular signaling pathwayGlial cell line-derived neurotrophic factor (GDN F), neurturin (NTN), persephin (PSP), and artemin (ART) are the members of a new family of neurotrophic factors distantly related to the members of the TGF␤ family (Lin et al

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Signaling pathways and survival effects of BDNF and NT-3 on cultured cerebellar granule cells

Cited by 92 publications

References 36 publications

Overcoming the Inhibitors of Myelin with a Novel Neurotrophin Strategy

Overcoming the Inhibitors of Myelin with a Novel Neurotrophin Strategy

Image-Based High-Content Screening in Drug Discovery

Receptors of the Glial Cell Line-Derived Neurotrophic Factor Family of Neurotrophic Factors Signal Cell Survival through the Phosphatidylinositol 3-Kinase Pathway in Spinal Cord Motoneurons

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