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Nat Commun. 2016 May 26;7:11725. doi: 10.1038/ncomms11725.

BDNF rescues BAF53b-dependent synaptic plasticity and cocaine-associated memory in the nucleus accumbens.

White AO1,2,3, Kramár EA1,2,3, López AJ1,2,3, Kwapis JL1,2,3,4, Doan J1,2,3, Saldana D1,2,3, Davatolhagh MF5, Alaghband Y1,2,3, Blurton-Jones M1,4,6, Matheos DP1,2,3, Wood MA1,2,3,4.

Author information

301 Qureshey Research Lab, Department of Neurobiology and Behavior, University of California, Irvine, California 92697, USA.
Center for the Neurobiology of Learning and Memory, Irvine, California 92697, USA.
Irvine Center for Addiction Neuroscience (ICAN), University of California, Irvine, California 92697, USA.
Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California 92697, USA.
Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Sue and Bill Gross Stem Cell Research Center, University of California, Irvine, California 92697, USA.


Recent evidence implicates epigenetic mechanisms in drug-associated memory processes. However, a possible role for one major epigenetic mechanism, nucleosome remodelling, in drug-associated memories remains largely unexplored. Here we examine mice with genetic manipulations targeting a neuron-specific nucleosome remodelling complex subunit, BAF53b. These mice display deficits in cocaine-associated memory that are more severe in BAF53b transgenic mice compared with BAF53b heterozygous mice. Similar to the memory deficits, theta-induced long-term potentiation (theta-LTP) in the nucleus accumbens (NAc) is significantly impaired in slices taken from BAF53b transgenic mice but not heterozygous mice. Further experiments indicate that theta-LTP in the NAc is dependent on TrkB receptor activation, and that BDNF rescues theta-LTP and cocaine-associated memory deficits in BAF53b transgenic mice. Together, these results suggest a role for BAF53b in NAc neuronal function required for cocaine-associated memories, and also that BDNF/TrkB activation in the NAc may overcome memory and plasticity deficits linked to BAF53b mutations.

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