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Journal of Neuroscience, Vol 16, 886-898, Copyright © 1996 by Society for Neuroscience
Fibroblast growth factor-2 protects entorhinal layer II glutamatergic neurons from axotomy-induced death
DA Peterson, CA Lucidi-Phillipi, DP Murphy, J Ray and FH Gage
Laboratory of Genetics, Salk Institute, La Jolla, California 92037, USA.
The entorhinal cortex is a major relay between the hippocampus and other
cortical and subcortical regions. Glutamatergic axons from layer II neurons
form the entorhinal cortical projection to the hippocampus via the
perforant pathway. We have demonstrated previously that lesion of the
perforant pathway causes the death of approximately 30% of entorhinal layer
II (ECL2) neurons. To elucidate mechanisms contributing to neuronal death
and to investigate strategies preventing it, we identified the phenotype of
the vulnerable neuronal population. Sections were immunolabeled with
antibodies to the neuronal markers NeuN, glutamate, and calbindin-D28k, and
to receptors for fibroblast growth factor-2 (FGFR1) and NMDA (NMDAR1) and
were examined using confocal microscopy. Calbindin immunoreactivity was
strikingly lamina- specific to ECL2, where one-third of all ECL2 neurons
were calbindin- positive. Localization of glutamate revealed that half of
the glutamatergic ECL2 neurons coexpressed calbindin. Quantification using
unbiased stereology at 9 weeks after lesion of the perforant pathway
revealed that the only ECL2 neuronal population that experienced a
significant (70%) loss (20% of the total) was the population of
glutamatergic ECL2 neurons that did not coexpress calbindin. All ECL2
neurons expressed FGFR1; therefore, we tested the role of FGF-2 in the
survival of glutamatergic ECL2 neurons. We grafted fibroblasts genetically
engineered to express nerve growth factor or FGF-2 and found that only
FGF-2 grafts prevented loss of the vulnerable
glutamatergic/calbindin-negative neurons. We present a hypothesis for the
selective vulnerability of these glutamatergic/calbindin-negative ECL2
neurons and address the role of FGF-2 in neuronal rescue.
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