BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA - A supportive role for nitric oxide?
2001 | journal article; research paper. A publication with affiliation to the University of Göttingen.
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Klocker, N., M. Jung, Claudia A. O. Stuermer, and Mathias Bähr. "BDNF increases the number of axotomized rat retinal ganglion cells expressing GAP-43, L1, and TAG-1 mRNA - A supportive role for nitric oxide?." Neurobiology of Disease 8, no. 1 (2001): 103-113. https://doi.org/10.1006/nbdi.2000.0329.
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- Authors
- Klocker, N.; Jung, M.; Stuermer, Claudia A. O.; Bähr, Mathias
- Abstract
- The death of neurons and the limited ability to activate growth-associated genes prevent the restoration of lesioned fiber tracts in the adult mammalian CNS. Here, we characterized the effects of the survival-promoting neurotrophin brain-derived neurotrophic factor (BDNF) on mRNA expression of GAP-43, L1, TAG-1, and SC-1 in axotomized and regenerating rat retinal ganglion cells (RGCs). BDNF led to de novo upregulation of TAG-1 mRNA in axotomized RGCs and to a threefold increase in the number of GAP-43 and L1 mRNA-expressing RGCs. SC-1 expression remained unchanged. However, BDNF did not improve long-distance axon regeneration into a peripheral nerve graft. Surprisingly, potentiating BDNF-mediated neuroprotection by simultaneous administration of a spin trap or a NOS inhibitor counteracted the BDNF-induced growth-associated gene expression. This led us to hypothesize that the BDNF effects on GAP-43, L1, and TAG-1 mRNA expression are mediated by a NO-dependent mechanism. In summary, our data support the idea that survival and axon regeneration of lesioned CNS neurons can be regulated independently. (C) 2001 Academic Press.
- Issue Date
- 2001
- Publisher
- Academic Press Inc
- Journal
- Neurobiology of Disease
- ISSN
- 0969-9961