INVESTIGADORES
ARREGUI Carlos Oscar
artículos
Título:
Brain-derived neurotrophic factor modulates GAP-43 but not Talfa1 expression in injured retinal ganglion cells of adults rats
Autor/es:
FOURNIER, A; BEER, J; ARREGUI, CO; ESSAGIAN, C; AGUAYO, AJ; MCKERRACHER, L; CARLOS OSCAR ARREGUI
Revista:
JOURNAL OF NEUROSCIENCE RESEARCH
Editorial:
Wiley Interscience
Referencias:
Año: 1997 vol. 47 p. 561 - 572
ISSN:
0360-4012
Resumen:
The administration of neurotrophins affects neuronal
survival and growth, but less is known about their
ability to modify the expression of growth associated
genes following injury to CNS neurons. Here we
characterize the effect of brain-derived neurotrophic
factor (BDNF) on mRNA levels for Ta1 a-tubulin,
and for GAP-43, two genes whose expression levels in
retinal ganglion cells (RGC) tend to correlate with
growth.We first determined that most adult rat RGCs
can retrogradely transport BDNF by injecting 125IBDNF
into RGC target sites in vivo. We then used
quantitative in situ hybridization to characterize the
effect of axotomy, or axotomy and BDNF administration
on mRNA levels for GAP-43 and Ta1. Axotomy
alone resulted in a general decrease in Ta1 a-tubulin
mRNA levels by 2 weeks, and elicited an increase in
GAP-43 mRNA levels in an average of 30% of
surviving RGCs. The intravitreal administration of a
single dose of BDNF (5 mg) to axotomized RGCs on
the day of injury did not affect Ta1 a-tubulin mRNA
levels, but was followed by a moderate (approximately
80%), and short-lasting enhancement of GAP-43
mRNAlevels in most RGCs during the first week after
axotomy. No significant increase in GAP-43 mRNA
levels was observed when BDNF was injected into the
uninjured eye. We conclude that BDNF specifically
enhances GAP-43 but not Ta1 mRNAlevels in injured
RGCs. Because BDNF is known to stimulate branch
length of injured RGCs, we suggest that changes in the
expression of GAP-43, but not Ta1 tubulin, correlate
with branching of injured neurons as opposed to long
distance regrowth.