Affiliations: [a]
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
| [b]
The Institutes of Brain Science, The State Key Laboratory of Medical Neurobiology, and The Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China
| [c]
Neurobiology/Aging Program, Life Sciences Institute (LSI), National University of Singapore, Singapore
Correspondence:
[*]
Correspondence to: Dr. Sreedharan Sajikumar, 2 MedicalDrive, MD9, Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore-117 597. E-mail: [email protected].
Abstract: 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.
