Editor's Summary
7 May 2009
Chromatin memory
Previous work has identified chromatin modification via histone acetylation as a facilitator of learning and memory processes, based on the administration of histone deacetylase (HDAC) inhibitors in rodent models. Now experiments in mice show that the neuronal levels of HDAC2, but not HDAC1, are inversely related to synaptic plasticity, memory formation and the induction of dendritic structural changes associated with memory. In addition, HDAC2 specifically associates with genes believed to be involved in plasticity and memory, whereas HDAC1 does not. These findings raise the possibility that drugs targeted at HDAC2 — rather than HDAC1 — might be of value in the treatment of human diseases associated with memory loss.
Article: HDAC2 negatively regulates memory formation and synaptic plasticity
Ji-Song Guan, Stephen J. Haggarty, Emanuela Giacometti, Jan-Hermen Dannenberg, Nadine Joseph, Jun Gao, Thomas J. F. Nieland, Ying Zhou, Xinyu Wang, Ralph Mazitschek, James E. Bradner, Ronald A. DePinho, Rudolf Jaenisch & Li-Huei Tsai
doi:10.1038/nature07925
Abstract | Full Text | PDF (1,205K) | Supplementary information
