Sequential Interactions of Fibroblast Growth Factor-2, Brain-Derived Neurotrophic Factor, Neurotrophin-3, and Their Receptors Define Critical Periods in the Development of Cochlear Ganglion Cells

2002 ◽  
Vol 175 (1) ◽  
pp. 138-151 ◽  
Author(s):  
W.Amin Hossain ◽  
C.L. Brumwell ◽  
D.K. Morest
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Neurotrophic Factor ◽  
Ganglion Cells ◽  
Brain Derived Neurotrophic Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Critical Periods ◽  
Neurotrophin 3

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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