Chromatin Acetylation, Memory, and LTP Are Impaired in CBP+/− Mice A Model for the Cognitive Deficit in Rubinstein-Taybi Syndrome and Its Amelioration

@article{Alarcon2004ChromatinAM,
  title={Chromatin Acetylation, Memory, and LTP Are Impaired in CBP+/− Mice A Model for the Cognitive Deficit in Rubinstein-Taybi Syndrome and Its Amelioration},
  author={Juan M Alarcon and Ga{\"e}l Malleret and Khalid Touzani and Svetlana Vronskaya and Shunsuke Ishii and Eric R. Kandel and Angel Barco},
  journal={Neuron},
  year={2004},
  volume={42},
  pages={947-959}
}
We studied a mouse model of the haploinsufficiency form of Rubinstein-Taybi syndrome (RTS), an inheritable disorder caused by mutations in the gene encoding the CREB binding protein (CBP) and characterized by mental retardation and skeletal abnormalities. In these mice, chromatin acetylation, some forms of long-term memory, and the late phase of hippocampal long-term potentiation (L-LTP) were impaired. We ameliorated the L-LTP deficit in two ways: (1) by enhancing the expression of CREB… Expand
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