Effects of NGF, b-FGF, and cerebrolysin on water maze performance and on motor activity of rats: short- and long-term study
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
10082636
DOI
10.1006/nlme.1998.3877
PII: S1074-7427(98)93877-1
Knihovny.cz E-resources
- MeSH
- Amino Acids pharmacology MeSH
- Maze Learning drug effects MeSH
- Time Factors MeSH
- Frontal Lobe surgery MeSH
- Fibroblast Growth Factor 2 pharmacology MeSH
- Rats MeSH
- Nerve Growth Factors pharmacology MeSH
- Psychomotor Performance drug effects MeSH
- Aging drug effects MeSH
- Parietal Lobe surgery MeSH
- Water MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Amino Acids MeSH
- cerebrolysin MeSH Browser
- Fibroblast Growth Factor 2 MeSH
- Nerve Growth Factors MeSH
- Water MeSH
The effects of 14-day treatments with nerve growth factor (NGF), basic fibroblast growth factor (b-FGF), or the peptidergic drug Cerebrolysin on postlesion acquisition of a water maze task and on motor activity were evaluated. Rats were tested in the Morris water maze 14 days (early test) and 7 to 8 months (delayed test) after a bilateral lesion of the frontoparietal (sensorimotor) cortex. Only the rats treated with Cerebrolysin performed the water maze task at the level of the nonlesioned controls in the early test. No short-term effect of NGF (6.5 ng/14 days; 38 ng/ml) or b-FGF (17 ng/14 days; 100 ng/ml) treatment was found. The delayed test revealed that water maze performance was restored in rats treated with b-FGF in comparison with intact controls. The data showed that b-FGF can support or initiate processes in the CNS that lead to a delayed functional amelioration and/or compensation for a water maze performance deficit. NGF did not influence the acquisition impairment caused by a sensorimotor cortical lesion. Two-week administration of Cerebrolysin had a time-dependent influence: it attenuated the acquisition deficit and increased the motor activity of rats, both effects declined to the level of lesioned controls within 8 months.
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