Evidence that brain-derived neurotrophic factor is a trophic factor for motor neurons in vivo

Neuron ◽  
1993 ◽  
Vol 10 (3) ◽  
pp. 359-367 ◽  
Author(s):  
Vassilis E. Koliatsos ◽  
Richard E. Clatterbuck ◽  
John W. Winslow ◽  
Michelle H. Cayouette ◽  
Donald L. Prices
1991 ◽  
Vol 331 (1261) ◽  
pp. 259-262

In the developing vertebrate nervous system the survival of neurons becomes dependent on the supply of a neurotrophic factor from their targets when their axons reach these targets. To determine how the onset of neurotrophic factor dependency is coordinated with the arrival of axons in the target field, we have studied the growth and survival of four populations of cranial sensory neurons whose axons have markedly different distances to grow to reach their targets. Axonal growth rate both in vivo and in vitro is related to target distance; neurons with more distant targets grow faster. The onset trophic factor dependency in culture is also related to target distance; neurons with more distant targets survive longer before becoming trophic factor dependent. These data suggest that programmes of growth and survival in early neurons play an important role in coordinating the timing of trophic interactions in the developing nervous system.


2020 ◽  
Vol 15 (1) ◽  
pp. FNL38 ◽  
Author(s):  
Zarlascht Karmand ◽  
Hans-Peter Hartung ◽  
Oliver Neuhaus

Aim: To detect IFN β-1a-induced expression of brain-derived neurotrophic factor (BDNF) to undermine the hypothesis of IFN β-1a-associated neuroprotection in multiple sclerosis (MS). Methods: The influence of IFN β-1a on in vitro activated peripheral blood lymphocytes from healthy donors was tested. Proliferation analyses were made to detect T-cell growth. BDNF expression was measured by standard ELISA. To assess the influence of IFN β-1a on BDNF expression in vivo, BDNF serum levels of MS patients treated with IFN β-1a were compared with those of untreated patients. Results: IFN β-1a inhibited T-cell proliferation dose dependently. It induced BDNF expression at middle concentrations. MS patients treated with IFN β-1a exhibited significantly lower BDNF serum levels than untreated patients. Conclusion: IFN β-1a may promote neuroprotection by inducing BDNF expression, but its importance in vivo remains open.


Nature ◽  
1992 ◽  
Vol 360 (6406) ◽  
pp. 753-755 ◽  
Author(s):  
Qiao Yan ◽  
Jeffrey Elliott ◽  
William D. Snider

FEBS Letters ◽  
1992 ◽  
Vol 313 (2) ◽  
pp. 138-142 ◽  
Author(s):  
Hitoshi Okazawa ◽  
Miho Murata ◽  
Masahiko Watanabe ◽  
Masaki Kamei ◽  
Ichiro Kanazawa

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