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

André O. White, Enikö A. Kramár, Alberto J. López, Janine L. Kwapis, John Doan, David Saldana, M. Felicia Davatolhagh, Yasaman Alaghband, Mathew Blurton-Jones, Dina P. Matheos and Marcelo A. Wood ()
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André O. White: 301 Qureshey Research Lab, University of California
Enikö A. Kramár: 301 Qureshey Research Lab, University of California
Alberto J. López: 301 Qureshey Research Lab, University of California
Janine L. Kwapis: 301 Qureshey Research Lab, University of California
John Doan: 301 Qureshey Research Lab, University of California
David Saldana: 301 Qureshey Research Lab, University of California
M. Felicia Davatolhagh: Perelman School of Medicine at the University of Pennsylvania
Yasaman Alaghband: 301 Qureshey Research Lab, University of California
Mathew Blurton-Jones: 301 Qureshey Research Lab, University of California
Dina P. Matheos: 301 Qureshey Research Lab, University of California
Marcelo A. Wood: 301 Qureshey Research Lab, University of California

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms11725

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