Exogenous Basic Fibroblast Growth Factor and Nerve Growth Factor Enhance Sprouting of Acetylcholinesterase Positive Fibers in Denervated Rat Hippocampus

Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) were administered into the rat brain following unilateral fimbria-fornix transection. Both bFGF and NGF stimulated the sprouting of acetylcholinesterase (AChE) positive fibers in the hippocampus on the lesioned side. Furthermore, a small number of AChE-positive fibers were regenerated even when only the vehicle was administered. Rats treated with NGF as well as control group had only thin fibers, whereas those treated with bFGF had not only thin fibers but also thick fibers. These results indicate that intrinsic NGF is released and acts on damaged neurons directly, while bFGF acts them on directly and/or indirectly after brain injury.</p

Delayed Precursor Cell Markers Expression in Hippocampus following Cold-Induced Cortical Injury in Mice

The purpose of this study was to examine the possibility of neuronal remodeling and repair after cold-induced brain injury using immunoassay of nestin and 3CB2 (potential precursor cell markers). Male ddN strain mice were subjected to cold-induced cortical injury. Animals were divided into the following six groups: (1) 1 day after injury, (2) 1 week after injury, (3) 2 weeks after injury, (4) 1 month after injury, (5) sham controls, and (6) normal controls. Western blot analysis (n = 3 in each group) and histological examination (n = 5 in each group) were performed. At 1 day and 1 week after injury, TUNEL-positive cells were observed, while immunoreactivity of nestin and 3CB2 was absent. At 1 month after injury, expression of both nestin and 3CB2 was observed in the ipsilateral hippocampus. Nestin was expressed in GFAP- or 3CB2-positive astrocytes at 1 month after injury, and nestin expression with TUC-4 (immature neuron marker) was present in the hippocampal cell layer. The findings demonstrate delayed nestin expression in both glia and neuronlike cells after brain injury. The present study suggests that the delayed nestin expression in glia and neuron-like cells might be part of the adaptation to injury.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63371/1/neu.2004.21.1747.pd