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Acidic Fibroblast Growth Factor Infusion Reduces Ischemic CA1 Hippocampal Damage in the Gerbil

Published online by Cambridge University Press:  18 September 2015

V. MacMillan ,
K. Walton-Roche  and
J. Davis
V. MacMillan*
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.) and the Department of Medicine (Neurology). Duke University, Durham, North Carolina (K.W-R, J.D.)
K. Walton-Roche
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.) and the Department of Medicine (Neurology). Duke University, Durham, North Carolina (K.W-R, J.D.)
J. Davis
Affiliation:
Division of Neurology, University of Toronto, Toronto (V.M.) and the Department of Medicine (Neurology). Duke University, Durham, North Carolina (K.W-R, J.D.)
*
Room 6366, Medical Science Building, University of Toronto, Toronto, Ontario, Canada M5S 1A8
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Abstract:

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Occlusion of the carotid arteries for 5 minutes in the Mongolian gerbil results in selective necrosis of CAI pyramidal neurons. In the present experiments we studied whether intraventricular infusion of acidic fibroblast growth factor (aFGF) could attentuate this damage. Intraventricular infusions of bovine serum albumin (BSA-10 ng/h) or aFGF (1, 10 or 100 ng/h) were started 2 days prior to 5 minutes of bilateral carotid occlusion and continued for 5 days post-ischemia. The brains were perfused and fixed at 5 days post-ischemia and histological assessment of CAI damage was made. Animals receiving intraventricular infusions of 10 or 100 ng/h aFGF showed a significant reduction of CA1 neuronal damage in comparison to no treatment ischemic controls (no treatment − 8 + 1 ; aFGF 10 ng/h − 147 ± 28; aFGF 100 ng/h − 168 ± 35 cells/mm CAI; P < 0.05 for both aFGF groups). The results indicate that aFGF infusion can attenuate the severity of ischemic neuronal necrosis in the gerbil hippocampus.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 20 , Issue 1 , February 1993 , pp. 37 - 40
Copyright
Copyright © Canadian Neurological Sciences Federation 1993

References

1.Mattson, MP, Murrain, M, Guthrie, PB, et al.Fibroblast growth factor and glutamate: opposing roles in the generation and degeneration of hippocampal neuroarchitecture. J Neurosci 1989: 9: 3728–3740.CrossRefGoogle ScholarPubMed
2.Rothman, SM, and Olney, JW.Glutamate and the pathophysiology of hypoxic-ischemic brain damage. Ann Neurol 1986: 19: 105–111.CrossRefGoogle ScholarPubMed
3.Choi, DW, Ionic dependence of glutamate neurotoxicity. J Neurosci 1987; 7: 369–379.CrossRefGoogle ScholarPubMed
4.Choi, DW, Glutamate neurotoxicity and diseases of the central nervous system. Neuron 1988; 1: 623–634.CrossRefGoogle Scholar
5.Jaye, M, Howk, R, Burgess, W, et al.Human endothelial cell growth factor: cloning, nucleotide sequence, and chromosomal localization. Science 1986; 233: 541–544.CrossRefGoogle Scholar
6.Crain, BJ, Westerkam, WD, Harrison, AH, et al.Selective neuronal death after transient forebrain ischemia in the Mongolian gerbil: a silver impregnation study. Neurosci 1988: 27: 387–402.Google Scholar
7.Loskota, WJ, Lomax, P, Verity, MA.A Stereotaxic Atlas of the Mongolian Gerbil Brain. Ann Arbor Science Publishers Inc: Ann Arbor, MI, 1974.Google Scholar
8.Wiliams, LR, Varon, S, Peterson, GM, et al.Continuous infusion of nerve growth factor prevents basal forebrain neuronal death after fimbria fornix transection. Proc Natl Acad Sci (USA) 1986: 83: 9231–9235.CrossRefGoogle Scholar
9.Hefti, F.Nerve growth factor promotes survival of septal cholinergic neurons after fimbrial transections. J Neurosci 1986; 6: 2155–2162.CrossRefGoogle ScholarPubMed
10.Kromer, LF.Nerve growth factor treatment after brain injury prevents neuronal death. Science 1987; 235: 214–216.CrossRefGoogle ScholarPubMed
11.Anderson, KJ, Dam, D, Lee, S, et al.Basic fibroblast growth factor prevents death of lesioned cholinergic neurons in vivo. Nature 1988; 332: 360–361.CrossRefGoogle ScholarPubMed
12.Yamada, K, Kinoshita, A, Kohmura, E, et al.Basic fibroblast growth factor prevents thalamic degeneration after cortical infarction. J Cereb Blood Flow Metab 1991; 11: 472–478.CrossRefGoogle ScholarPubMed
13.Date, I, Notter, MFD, Felten, SY, et al.MPTP - treated young mice but not aging mice show partial recovery of the nigro-strialal dopaminergic system by stereotaxic injection of acidic fibroblast growth factor (aFGF). Brain Res 1990; 526: 156–160.CrossRefGoogle Scholar
14.Oomura, Y, Sasaki, K, Muto, T, et al.Physiological actions of fibroblast growth factor (FGF) in central nervous system. Soc Neurosci Abstr 1990; 16: 516.Google Scholar
15.Gospodarowicz, D.Molecular and developmental biology aspects of fibroblast growth factor. In: JE, Kudlow, DH, MacLennan, A, Bernstein, AJ, Gotlieb, eds. Biology of Growth Factors. New York: Plenum Publishing Corp, 1988; Vol 5: 23–39.CrossRefGoogle Scholar
16.Walicke, PA.Basic and acidic fibroblast growth factors have trophic effects on neurons from multiple CNS regions. J Neurosci 1988; 8: 2618–2627.CrossRefGoogle ScholarPubMed
17.Finklestein, SP, Apostolides, PJ, Caday, CG, et al.Increased basic fibroblast growth factor (bFGF) immunoreactivily at the site of focal brain wounds. Brain Res 1988; 460: 253–259.CrossRefGoogle ScholarPubMed
18.Finklestein, SF, Fanning, PJ, Caday, CG, et al.Increased levels of basic fibroblast growth factor (bFGF) following focal brain injury. Rest Neurol and Neurosci 1990; 1: 387–394.Google ScholarPubMed
19.Shigeno, T.Yamasaki, Y, Kalo, G, et al.Reduction of delayed neuronal death by inhibition of protein synthesis. Neurosci Lett 1990; 120: 117–119.CrossRefGoogle ScholarPubMed
20.Busto, R, Dietrich, WD.Globus, M. Y-T, et al.Post-ischemic moderate hypothermia inhibits CAI hippocampal ischemic neuronal injury. Neurosci Lett 1989; 101: 299–304.CrossRefGoogle Scholar
21.Buchan, A and Pulsinelli, WA.Hypothermia but not the N-methyl-D-asparate antagonist, MK-801, attenuates neuronal damage in gerbils subjected to transient global ischemia. J. Neurosci 1990; 10: 311–316.CrossRefGoogle ScholarPubMed