PHOTOCHEMICALLY INDUCED FOCAL CEREBRAL-ISCHEMIA IN RAT - TIME-DEPENDENT AND GLOBAL INCREASE IN EXPRESSION OF BASIC FIBROBLAST GROWTH-FACTORMESSENGER-RNA
A. Lippoldt et al., PHOTOCHEMICALLY INDUCED FOCAL CEREBRAL-ISCHEMIA IN RAT - TIME-DEPENDENT AND GLOBAL INCREASE IN EXPRESSION OF BASIC FIBROBLAST GROWTH-FACTORMESSENGER-RNA, Brain research, 625(1), 1993, pp. 45-56
Induction of basic fibroblast growth factor (bFGF) mRNA expression was
studied in a Rose bengal induced focal cerebral ischemia during a tim
e course of 2, 4, 24, 72 h and 7 days. Focal cerebral ischemia induced
by Rose bengal resulted in a global upregulation in bFGF gene express
ion at the 24 h time-interval. This upregulation in bFGF gene expressi
on was due to an upregulation in glial bFGF expression in most of the
areas studied as seen by means of non-radioactive in situ hybridizatio
n in combination with immunocytochemistry for glial fibrillary acidic
protein. However, in the piriform cortex a putative neuronal upregulat
ion of bFGF could be detected by combination of non-radioactive in sit
u hybridization, immunohistochemistry for glial fibrillary acidic prot
ein and nuclear staining with Neutral red. Semiquantitative data conce
rning bFGF mRNA expression were obtained by use of computer-assisted m
icrodensitometry and revealed substantial increases in bFGF mRNA expre
ssion in the cingulate cortex, the neostriatum, a 1 mm marginal zone c
lose to the external capsule and the olfactory tubercle at bregma leve
ls 1 to 2 mm rostral to the lesion. No changes in bFGF gene expression
were seen in field CA1 of Ammon's horn on the lesioned side and in de
ntate gyrus at bregma levels between - 2.12 to - 3.30 mm. We observed
significant changes in bFGF upregulation in the caudate putamen, the p
iriform cortex and the amygdaloid region and the frontoparietal cortex
at bregma levels - 2.12 to - 3.30 mm. These data indicate that photoc
hemically induced focal cerebral ischemia leads to an early and global
response in bFGF gene expression, which is due to an upregulation mai
nly in astrocytes. The observed widespread upregulation of the bFGF ge
ne transcription rostral and caudal to the lesion is suggested to be d
ue in part to neuronal glutaminergic connections between the areas inv
estigated and in part due to increases in extracellular fluid signals
(volume transmission).