scholarly journals Immunohistochemical Localization of Brain-derived Neurotrophic Factor in the Spinal Cords of Amyotrophic Lateral Sclerosis and Non-Amyotrophic Lateral Sclerosis Patients

1998 ◽  
Vol 57 (9) ◽  
pp. 822-830 ◽  
Author(s):  
Yasuhiro Kawamoto ◽  
Shinichi Nakamura ◽  
Ichiro Akiguchi ◽  
Jun Kimura
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Immunohistochemical Localization ◽  
Lateral Sclerosis

Antiapoptotic activity maintenance of Brain Derived Neurotrophic Factor and the C fragment of the tetanus toxin genetic fusion protein

2008 ◽  
Vol 3 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jesús Ciriza ◽  
Marcos García-Ojeda ◽  
Inmaculada Martín-Burriel ◽  
Cendra Agulhon ◽  
Francisco Miana-Mena ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurotrophic Factor ◽  
Tetanus Toxin ◽  
Brain Derived Neurotrophic Factor ◽  
Trophic Factors ◽  
Low Concentrations ◽  
Neuro2a Cells ◽  
Genetic Fusion ◽  
The Brain ◽  
Lateral Sclerosis

AbstractNeurotrophic factors have been widely suggested as a treatment for multiple diseases including motorneuron pathologies, like Amyotrophic Lateral Sclerosis. However, clinical trials in which growth factors have been systematically administered to Amyotrophic Lateral Sclerosis patients have not been effective, owing in part to the short half-life of these factors and their low concentrations at target sites. A possible strategy is the use of the atoxic C fragment of the tetanus toxin as a neurotrophic factor carrier to the motorneurons. The activity of trophic factors should be tested because their genetic fusion to proteins could alter their folding and conformation, thus undermining their neuroprotective properties. For this purpose, in this paper we explored the Brain Derived Neurotrophic Factor (BDNF) activity maintenance after genetic fusion with the C fragment of the tetanus toxin. We demonstrated that BDNF fused with the C fragment of the tetanus toxin induces the neuronal survival Akt kinase pathway in mouse cortical culture neurons and maintains its antiapoptotic neuronal activity in Neuro2A cells.

The expression of trkB and p75 and the role of BDNF in the developing neuromuscular system of the chick embryo

Development ◽  
1996 ◽  
Vol 122 (2) ◽  
pp. 715-724 ◽  
Author(s):  
S.E. McKay ◽  
a. Garner ◽  
J. Caldero ◽  
R.P. Tucker ◽  
T. Large ◽  
...  
Keyword(s):  
Cell Death ◽  
Chick Embryo ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Immunohistochemical Localization ◽  
Neurotrophin Receptor ◽  
Lumbar Region ◽  
Temporal Shift ◽  
Motoneuron Cell

The neurotrophin, brain-derived neurotrophic factor, prevents motoneuron cell death during the normal development of the chick embryo. Brain-derived neurotrophic factor is a ligand for the low-affinity NGF receptor, p75, and for the high-affinity neurotrophin receptor, trkB. If motoneurons respond directly to brain-derived neurotrophic factor then they must possess at least one, and possibly both, of these receptors during the period of naturally occurring cell death. Histological sections from the lumbar region of chick embryos were probed for the presence of trkB and p75 mRNA using digoxigenin-labeled anti-sense RNA probes. p75 mRNA was present in spinal cord motoneurons at stages of development that correlate with motoneuron cell death. Immunohistochemical localization also revealed that p75 protein was present in motoneurons, primarily along the ventral roots and developing intramuscular nerves. In contrast trkB mRNA was not present in chick motoneurons until after the process of cell death was underway. The timing of trkB expression suggested that some motoneurons, i.e., those that die prior to the onset of trkB expression, may be insensitive to brain-derived neurotrophic factor. This was confirmed by comparing the number of surviving motoneurons following different in vivo treatment paradigms. The evidence indicates that motoneurons undergo a temporal shift in sensitivity to brain-derived neurotrophic factor.

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