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Rescuing impairment of long-term potentiation in fyn-deficient mice by introducing Fyn transgene.

To examine the physiological role of the Fyn tyrosine kinase in neurons, we generated transgenic mice that expressed a fyn cDNA under the control of the calcium/calmodulin-dependent protein kinase IIalpha promoter. With this promoter, we detected only low expression of Fyn in the neonatal brain. In contrast, there was strong expression of the fyn-transgene in neurons of the adult forebrain. To determine whether the impairment of long-term potentiation (LTP) observed in adult fyn-deficient mice was caused directly by the lack of Fyn in adult hippocampal neurons or indirectly by an impairment in neuronal development, we generated fyn-rescue mice by introducing the wild-type fyn-transgene into mice carrying a targeted deletion in the endogenous fyn gene. In fyn-rescue mice, Schaffer collateral LTP was restored, even though the morphological abnormalities characteristic of fyn-deficient mice were still present. These results suggest that Fyn contributes, at least in part, to the molecular mechanisms of LTP induction.

Pubmed ID: 9114065

Authors

  • Kojima N
  • Wang J
  • Mansuy IM
  • Grant SG
  • Mayford M
  • Kandel ER

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Data

April 29, 1997

Associated Grants

None

Mesh Terms

  • Age Factors
  • Animals
  • Hippocampus
  • Long-Term Potentiation
  • Mice
  • Mice, Transgenic
  • Neurons
  • Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-fyn
  • Proto-Oncogene Proteins pp60(c-src)