BDNF rescues BAF53b-dependent synaptic plasticity and cocaine-associated memory in the nucleus accumbens
Male
0301 basic medicine
Chromosomal Proteins, Non-Histone
1.1 Normal biological development and functioning
Knockout
Science
Biological Psychology
Long-Term Potentiation
610
Mice, Transgenic
Basic Behavioral and Social Science
Transgenic
Article
Nucleus Accumbens
Cell Line
Substance Misuse
Mice
Cocaine-Related Disorders
03 medical and health sciences
Cocaine
Behavioral and Social Science
Genetics
Psychology
2.1 Biological and endogenous factors
Animals
Receptor, trkB
Mice, Knockout
Memory Disorders
Biomedical and Clinical Sciences
Brain-Derived Neurotrophic Factor
Q
Neurosciences
Pharmacology and Pharmaceutical Sciences
Non-Histone
Brain Disorders
Chromosomal Proteins
Neurological
trkB
Female
Drug Abuse (NIDA only)
Receptor
DOI:
10.1038/ncomms11725
Publication Date:
2016-05-26T09:48:14Z
AUTHORS (11)
ABSTRACT
Abstract Recent evidence implicates epigenetic mechanisms in drug-associated memory processes. However, a possible role for one major mechanism, nucleosome remodelling, memories remains largely unexplored. Here we examine mice with genetic manipulations targeting neuron-specific remodelling complex subunit, BAF53b. These display deficits cocaine-associated that are more severe BAF53b transgenic compared heterozygous mice. Similar to the deficits, theta-induced long-term potentiation (theta-LTP) nucleus accumbens (NAc) is significantly impaired slices taken from but not Further experiments indicate theta-LTP NAc dependent on TrkB receptor activation, and BDNF rescues Together, these results suggest neuronal function required memories, also BDNF/TrkB activation may overcome plasticity linked mutations.
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CITATIONS (44)
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