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Basic fibroblast growth factor ameliorates learning deficits in basal forebrain-lesioned mice.
A Ishihara1, H Saito, N Nishiyama
1Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Japanese Journal of Pharmacology
|May 1, 1992
Summary
Basic fibroblast growth factor (bFGF) treatment improved memory and learning in mice with basal forebrain (BF) lesions. bFGF enhanced performance without altering cortical choline acetyltransferase (ChAT) activity, suggesting a specific effect on memory deficits.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Basal forebrain (BF) lesions in mice lead to significant impairments in memory and learning.
- Basic fibroblast growth factor (bFGF) is a protein with known roles in cell growth and survival.
- Investigating neurotrophic factors like bFGF is crucial for understanding and potentially treating cognitive deficits.
Purpose of the Study:
- To evaluate the therapeutic potential of basic fibroblast growth factor (bFGF) in ameliorating memory and learning deficits induced by basal forebrain (BF) lesions.
- To determine if bFGF treatment affects cognitive performance in a mouse model of BF-induced amnesia.
- To examine the impact of bFGF on cortical choline acetyltransferase (ChAT) activity following BF lesions.
Main Methods:
- Bilateral basal forebrain (BF) lesions were induced in adult male ddY mice using radiofrequency current.
- Basic fibroblast growth factor (bFGF) was administered via microinjection into the lesion site immediately after injury.
- Cognitive function was assessed using a step-through type passive avoidance test over 10 days, starting 15 days post-treatment.
- Cortical choline acetyltransferase (ChAT) activity was measured to assess cholinergic system integrity.
Main Results:
- BF-lesioned mice exhibited significant deficits in the acquisition phase of the passive avoidance task, while retention remained largely unaffected.
- Treatment with basic fibroblast growth factor (bFGF) dose-dependently improved step-through performance, indicated by elongated latencies and reduced acquisition times.
- bFGF administration did not reverse the decrease in cortical choline acetyltransferase (ChAT) activity caused by the BF lesions.
Conclusions:
- Basic fibroblast growth factor (bFGF) effectively ameliorates memory and learning impairments following basal forebrain (BF) lesions in mice.
- The memory-enhancing effects of bFGF occur independently of changes in cortical choline acetyltransferase (ChAT) activity.
- These findings highlight bFGF as a potential therapeutic agent for cognitive disorders associated with BF dysfunction.