Developmental and regional expression of basic fibroblast growth factor mRNA in the rat central nervous system

Ernfors, Patrik; Lönnerberg, Peter; Ayer-LeLièvre, Christiane; Persson, Håkan

doi:10.1002/jnr.490270103

Cited by 111 publications

(46 citation statements)

References 36 publications

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“…Northern analysis has suggested that bFGF mRNA is distributed widely throughout the brain (35), and immunohistochemical studies have reported localization of bFGF in neurons of the cerebral cortex, hippocampus, cerebellum (36)(37)(38), and in neuroglia (39). These data are in accord with our present observations suggesting a widespread distribution of bFGF in neurons and glial cells within brain.…”

Section: Discussionsupporting

confidence: 83%

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

Bean

Elde

Cao

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

116

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The distribution of acidic (aFGF) and basic (bFGF) fibroblast growth factor mRNA and protein were examined in mesencephalon by immunohistochemistry, immunoblot analysis, in situ hybridization histochemistry, and RNA analysis. Coexistence of aFGF or bFGF with tyrosine hydroxylase protein in nigral cells was observed with immunohistochemistry. Both aFGF and bFGF mRNAs were found in the substantia nigra. Unilateral 6-hydroxydopamine lesions of nigrostriatal neurons resulted in a loss of aFGF and tyrosine hydroxylase [L-tyrosine, tetrahydropteridine: oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] mRNA-positive neurons on the lesioned side. The distribution of aFGF mRNA in monkey brain was similar to that seen in the rat. RNA and immunoblot analysis confirmed the presence of both aFGF and bFGF mRNAs and proteins in the substantia nigra of rat, monkey, and human.

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Section: Discussionsupporting

confidence: 83%

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

Bean

Elde

Cao

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

116

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“…FGF-1 and FGF-2 are expressed in both developing and adult brain (Ernfors et al, 1990;Gonzalez et al, 1990;Kalcheim and Neufeld, 1990;Schnurch and Risau, 1991), and FGF-1 is associated with enhanced myelination after a demyelinating lesion (Tourbah et al, 1992). Although these studies are consistent with a role for FGF in C NS myelination, this has yet to be demonstrated in vivo.…”

Section: Abstract: Cns Development; Myelin; Oligodendrocyte; O-2a Prmentioning

confidence: 95%

Transplanted Oligodendrocyte Progenitor Cells Expressing a Dominant-Negative FGF Receptor Transgene Fail to MigrateIn Vivo

Osterhout¹,

Ebner²,

et al. 1997

J. Neurosci.

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The proliferation, migration, survival, and differentiation of oligodendrocyte progenitor cells, precursors to myelin-forming oligodendrocytes in the CNS, are controlled by a number of polypeptide growth factors in vitro. The requirement and roles for individual factors in vivo, however, are primarily unknown. We have used a cell transplantation approach to examine the role of fibroblast growth factor (FGF) in oligodendrocyte development in vivo. A dominant-negative version of the FGF receptor-1 transgene was introduced into oligodendrocyte progenitors in vitro, generating cells that were nonresponsive to FGF but responsive to other mitogens. When transplanted into the brains of neonatal rats, mutant cells were unable to migrate and remained within the ventricles. These results suggest a role for FGF signaling in establishing a motile phenotype for oligodendrocyte progenitor cell migration in vivo and illustrate the utility of a somatic cell mutagenesis approach for the study of gene function during CNS development in vivo.

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“…These factors were chosen because they are synthesized in the cerebellum and can promote survival of other neuronal populations (28)(29)(30)(31). Moreover, the receptors for all these factors are present in the cerebellar granule layer (17,19,32,33).…”

mentioning

confidence: 99%

Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP.

D’Mello

Galli

Ciotti

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

847

858

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High levels of extracellular K+ ensure proper development and prolong survival of cerebellar granule neurons in culture. We find that when switched from a culture medium containing high K+ (25 mM) to one containing a low but more physiological K+ concentration (5 mM), differentiated granule neurons degenerate and die. Death induced by low K+ is due to apoptosis (programmed cell death), a form of cell death observed extensively in the developing nervous system and believed to be necessary for proper neurogenesis. The death process is accompanied by cleavage of genomic DNA into internucleosome-sized fragments, a hallmark of apoptosis. Inhibitors of transcription and translation suppress apoptosis induced by low K+, suggesting the necessity for newly synthesized gene products for activation of the process. Death can be prevented by insulin-like growth factor I but not by several other growth/neurotrophic factors. cAMP but not the protein kinase C activator phorbol 12-myristate 13-acetate can also support survival in low K+. In view of the large numbers of granule neurons that can be homogeneously cultured, our results offer the prospect of an excellent model system to study the mechanisms underlying apoptosis in the central nervous system and the suppression of this process by survival factors such as insulin-like growth factor I.

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Developmental and regional expression of basic fibroblast growth factor mRNA in the rat central nervous system

Cited by 111 publications

References 36 publications

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human.

Transplanted Oligodendrocyte Progenitor Cells Expressing a Dominant-Negative FGF Receptor Transgene Fail to MigrateIn Vivo

Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP.

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