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Journal of Neuroscience, Vol 12, 345-355, Copyright © 1992 by Society for Neuroscience
Basic FGF in adult rat brain: cellular distribution and response to entorhinal lesion and fimbria-fornix transection
F Gomez-Pinilla, JW Lee and CW Cotman
Department of Psychobiology, University of California, Irvine 92717.
Basic fibroblast growth factor (bFGF) is a potent trophic factor for
neurons and astrocytes and recently has been implicated in the pathology of
Alzheimer's disease. In order to better understand the role of bFGF in
normal brain function and during pathology, we have analyzed its anatomical
distribution and its response to injury in the CNS. Double-staining
immunohistochemistry showed that bFGF immunoreactivity was localized in
astrocytes, in select neuronal populations, and occasionally in microglial
cells throughout the normal rat brain. Neuronal populations that showed
bFGF immunoreactivity included septohippocampal nucleus, cingulate cortex,
subfield CA2 of the hippocampus, cerebellar Purkinje cells, cerebellar deep
nuclei, facial nerve nucleus, and the motor and spinal subdivisions of the
trigeminal nucleus and facial nerve nucleus. The pattern of bFGF
immunoreactivity in the hippocampus was examined following entorhinal
cortex lesion, or fimbria-fornix transection. After entorhinal cortex
lesion, bFGF immunoreactivity increased in the outer molecular layer of the
dentate gyrus ipsilateral to the lesion. The lesion effect on bFGF
immunoreactivity was expressed as an increase in the number of bFGF
astrocytes, as an increase in the intensity of bFGF immunoreactivity within
astrocytes, and as an increase of bFGF immunoreactivity in the surrounding
extracellular matrix, relative to the contralateral side. The time course
and pattern of reorganization paralleled the sprouting of septal
cholinergic terminals in response to the same type of lesion, suggesting
that bFGF may play an important role in lesion-induced plasticity. After
transection of the fimbria-fornix, chronic infusion of bFGF appeared to
preserve NGF receptors on neurons within the medial septal complex and, as
previously reported, prevent the death of medial septal neurons. Therefore,
it appears that bFGF infusion, which has been shown to increase the
synthesis of NGF by astrocytes (Yoshida and Gage, 1991), also helps enable
neurons to respond to NGF. This suggests that after injury bFGF may
participate in a cascade of neurotrophic events, directly and indirectly
facilitating neuronal repair and/or promoting neuronal survival.
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