HDAC2 expression in parvalbumin interneurons regulates synaptic plasticity in the mouse visual cortex
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Author(s)
Nott, Alexander
Cho, Sukhee
Seo, Jinsoo
Tsai, Li-Huei
Date Issued
January 2015
Journal
Neuroepigenetics
Publisher
Elsevier
Citation
Nott, Alexi et al. “HDAC2 Expression in Parvalbumin Interneurons Regulates Synaptic Plasticity in the Mouse Visual Cortex.” Neuroepigenetics 1 (January 2015): 34–40 © 2014 The Authors
Abstract
An experience-dependent postnatal increase in GABAergic inhibition in the visual cortex is important for the closure of a critical period of enhanced synaptic plasticity. Although maturation of the subclass of parvalbumin (Pv)-expressing GABAergic interneurons is known to contribute to critical period closure, the role of epigenetics on cortical inhibition and synaptic plasticity has not been explored. The transcription regulator, histone deacetylase 2 (HDAC2), has been shown to modulate synaptic plasticity and learning processes in hippocampal excitatory neurons. We found that genetic deletion of HDAC2 specifically from Pv interneurons reduces inhibitory input in the visual cortex of adult mice and coincides with enhanced long-term depression that is more typical of young mice. These findings show that HDAC2 loss in Pv interneurons leads to a delayed closure of the critical period in the visual cortex and supports the hypothesis that HDAC2 is a key negative regulator of synaptic plasticity in the adult brain.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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Creative Commons Attribution 3.0 Unported license
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DOI of Published Version
https://doi.org/10.1016/J.NEPIG.2014.10.005
