%0 Journal Article %J J Alzheimers Dis %D 2016 %T Inhibition of Histone Deacetylase 3 Restores Amyloid-β Oligomer-Induced Plasticity Deficit in Hippocampal CA1 Pyramidal Neurons. %A Krishna, Kumar %A Behnisch, Thomas %A Sajikumar, Sreedharan %K Acrylamides %K Alzheimer Disease %K Amyloid beta-Peptides %K Animals %K Excitatory Postsynaptic Potentials %K Hippocampus %K Histone Deacetylase Inhibitors %K Histone Deacetylases %K Long-Term Potentiation %K Male %K Patch-Clamp Techniques %K Peptide Fragments %K Phenylenediamines %K Pyramidal Cells %K Rats, Wistar %K Tissue Culture Techniques %X

Neurodegenerative diseases such as Alzheimer's disease (AD) are associated with alterations in epigenetic factors leading to cognitive decline. Histone deacetylase 3 (HDAC3) is a known critical epigenetic negative regulator of learning and memory. In this study, attenuation of long-term potentiation by amyloid-β oligomer, and its reversal by specific HDAC3 inhibitor RGFP966, was performed in rat CA1 pyramidal neurons using whole cell voltage-clamp and field recording techniques. Our findings provide the first evidence that amyloid-β oligomer-induced synaptic plasticity impairment can be prevented by inhibition of HDAC3 enzyme both at the single neuron as well as in a population of neurons, thus identifying HDAC3 as a potential target for ameliorating AD related plasticity impairments.

%B J Alzheimers Dis %V 51 %P 783-91 %8 2016 %G eng %N 3 %1 http://www.ncbi.nlm.nih.gov/pubmed/26890755?dopt=Abstract %R 10.3233/JAD-150838