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
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.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (59)
CITATIONS (44)