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Acidic and basic fibroblast growth factor mRNAs are increased in striatum following MPTP-induced dopamine neurofiber
Abstract:
Acidic fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF), the two best characterized members of a growing family of heparin-binding growth factors, have been shown to affect both survival of cultured neurons and regeneration of nerve terminals when applied exogenously. The endogenous expression of these growth factors in response to brain injury is not well understood. We have utilized the Swiss-Webster mouse, treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and a quantitative polymerase chain reaction assay to examine changes in endogenous synthesis of mRNA for both aFGF and bFGF in the striatum and substantia nigra. We have found that MPTP treatment results in a loss of 95% of dopaminergic function and is accompanied by an increase in expression of both aFGF and bFGF in the striatum at 1 week post-lesion. After 5 weeks, the terminals appear to be regenerating and FGF mRNA expression has returned to control levels. These results suggest that cellular reaction to chemical lesion in the brain may involve changes in growth factor expression, including both aFGF and bFGF.
Insights
Brain injury increases acidic and basic fibroblast growth factors (aFGF and bFGF) in mice. FGF mRNA levels return to normal as nerve terminals regenerate, suggesting a role for these growth factors in brain repair.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Acidic fibroblast growth factor (aFGF) and basic fibroblast growth factor (bFGF) are key heparin-binding growth factors.
- These factors influence neuronal survival and nerve terminal regeneration.
- Endogenous expression of aFGF and bFGF following brain injury remains poorly understood.
Purpose of the Study:
- To investigate changes in endogenous aFGF and bFGF mRNA expression in response to neurotoxin-induced brain injury.
- To examine the role of FGFs in the context of dopaminergic neuron damage and regeneration.
Main Methods:
- Utilized Swiss-Webster mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce brain injury.
- Employed quantitative polymerase chain reaction (qPCR) to measure aFGF and bFGF mRNA levels.
- Analyzed mRNA expression in the striatum and substantia nigra.
Main Results:
- MPTP treatment caused a 95% loss of dopaminergic function.
- Striatal expression of both aFGF and bFGF mRNA significantly increased at 1 week post-lesion.
- FGF mRNA levels returned to control levels by 5 weeks, coinciding with nerve terminal regeneration.
Conclusions:
- Cellular responses to chemical brain lesions involve alterations in growth factor expression, including aFGF and bFGF.
- These findings suggest a potential role for FGFs in the brain's response to injury and subsequent repair processes.