Ciliary Neurotrophic Factor Activates Spinal Cord Astrocytes, Stimulating Their Production and Release of Fibroblast Growth Factor-2, to Increase Motor Neuron Survival

2002 ◽  
Vol 173 (1) ◽  
pp. 46-62 ◽  
Author(s):  
Phillip J. Albrecht ◽  
John P. Dahl ◽  
Olivia K. Stoltzfus ◽  
Robert Levenson ◽  
Steven W. Levison
Keyword(s):  
Spinal Cord ◽  
Growth Factor ◽  
Motor Neuron ◽  
Fibroblast Growth Factor ◽  
Neurotrophic Factor ◽  
Ciliary Neurotrophic Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Neuron Survival ◽  
Motor Neuron Survival

scholarly journals Hepatocyte Growth Factor Promotes Motor Neuron Survival and Synergizes with Ciliary Neurotrophic Factor

1997 ◽  
Vol 272 (8) ◽  
pp. 5187-5191 ◽  
Author(s):  
Vivien Wong ◽  
David J. Glass ◽  
Ruth Arriaga ◽  
George D. Yancopoulos ◽  
Ronald M. Lindsay ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Motor Neuron ◽  
Neurotrophic Factor ◽  
Ciliary Neurotrophic Factor ◽  
Neuron Survival ◽  
Motor Neuron Survival ◽  
Hepatocyte Growth

scholarly journals Localized delivery of fibroblast growth factor–2 and brain-derived neurotrophic factor reduces spontaneous seizures in an epilepsy model

2009 ◽  
Vol 106 (17) ◽  
pp. 7191-7196 ◽  
Author(s):  
Beatrice Paradiso ◽  
Peggy Marconi ◽  
Silvia Zucchini ◽  
Elena Berto ◽  
Anna Binaschi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Neurotrophic Factor ◽  
Viral Vectors ◽  
Neuronal Damage ◽  
Brain Derived Neurotrophic Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Damage Limitation

A loss of neurons is observed in the hippocampus of many patients with epilepsies of temporal lobe origin. It has been hypothesized that damage limitation or repair, for example using neurotrophic factors (NTFs), may prevent the transformation of a normal tissue into epileptic (epileptogenesis). Here, we used viral vectors to locally supplement two NTFs, fibroblast growth factor–2 (FGF-2) and brain-derived neurotrophic factor (BDNF), when epileptogenic damage was already in place. These vectors were first characterized in vitro, where they increased proliferation of neural progenitors and favored their differentiation into neurons, and they were then tested in a model of status epilepticus-induced neurodegeneration and epileptogenesis. When injected in a lesioned hippocampus, FGF-2/BDNF expressing vectors increased neuronogenesis, embanked neuronal damage, and reduced epileptogenesis. It is concluded that reduction of damage reduces epileptogenesis and that supplementing specific NTFs in lesion areas represents a new approach to the therapy of neuronal damage and of its consequences.

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