Fibroblast growth factor-2 protects entorhinal layer II glutamatergic neurons from axotomy-induced death

摘要: The entorhinal cortex is a major relay between the hippocampus and other cortical subcortical regions. Glutamatergic axons from layer II neurons form projection to via perforant pathway. We have demonstrated previously that lesion of pathway causes death approximately 30% (ECL2) neurons. To elucidate mechanisms contributing neuronal investigate strategies preventing it, we identified phenotype vulnerable population. Sections were immunolabeled with antibodies markers NeuN, glutamate, calbindin-D28k, receptors for fibroblast growth factor-2 (FGFR1) NMDA (NMDAR1) examined using confocal microscopy. Calbindin immunoreactivity was strikingly lamina-specific ECL2, where one-third all ECL2 calbindin-positive. Localization glutamate revealed half glutamatergic coexpressed calbindin. Quantification unbiased stereology at 9 weeks after only population experienced significant (70%) loss (20% total) did not coexpress All expressed FGFR1; therefore, tested role FGF-2 in survival grafted fibroblasts genetically engineered express nerve factor or found grafts prevented glutamatergic/calbindin-negative present hypothesis selective vulnerability these address rescue.