Evidence map›Paper›PMID 21521655›Full record

ReviewNeurobiology of learning and memory2011

HDAC3 and the molecular brake pad hypothesis.

Susan C McQuown, Marcelo A Wood

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of learning and memory, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

80 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Epigenetic manipulation of anterior insular cortex alters neural signals and cognitive control.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. HDAC3 Activity within the Nucleus Accumbens Regulates Cocaine-Induced Plasticity and Behavior in a Cell-Type-Specific Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  18. Article
  19. Article
  20. Review

20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Susan C McQuownUniversity of California, Irvine, Department of Neurobiology and Behavior, Center for the Neurobiology of Learning and Memory, Institute for Memory Impairments and Neurological Disorders, United States.
Marcelo A Wood
University of California, Irvine · US

Funding

Behavioral and Epigenetic Mechanisms in Extinction of Cocaine-Induced MemoriesR01DA025922 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI LATTAL, K MATTHEW, WOOD, MARCELO ANDRES · 2008 to 2018
$5.1M
Chromatin Remodeling and Memory StorageR01MH081004 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI WOOD, MARCELO ANDRES · 2008 to 2012
$1.9M
NIDA NIH HHS R01 DA025922NIDA NIH HHS R01DA025922NIMH NIH HHS R01 MH081004NIMH NIH HHS R01MH081004
6 · The paper itself

Abstract

Successful transcription of specific genes required for long-term memory processes involves the orchestrated effort of not only transcription factors, but also very specific enzymatic protein complexes that modify chromatin structure. Chromatin modification has been identified as a pivotal molecular mechanism underlying certain forms of synaptic plasticity and memory. The best-studied form of chromatin modification in the learning and memory field is histone acetylation, which is regulated by histone acetyltransferases and histone deacetylases (HDACs). HDAC inhibitors have been shown to strongly enhance long-term memory processes, and recent work has aimed to identify contributions of individual HDACs. In this review, we focus on HDAC3 and discuss its recently defined role as a negative regulator of long-term memory formation. HDAC3 is part of a corepressor complex and has direct interactions with Class II HDACs that may be important for its molecular and behavioral consequences. And last, we propose the "molecular brake pad" hypothesis of HDAC function. The HDACs and associated corepressor complexes may function in neurons, in part, as "molecular brake pads." HDACs are localized to promoters of active genes and act as a persistent clamp that requires strong activity-dependent signaling to temporarily release these complexes (or brake pads) to activate gene expression required for long-term memory formation. Thus, HDAC inhibition removes the "molecular brake pads" constraining the processes necessary for long-term memory and results in strong, persistent memory formation.

Indexed as

AcetylationAnimalsChromatinEpigenesis, GeneticHistone Deacetylase 3Histone DeacetylasesLearningMemory, Long-TermChromatinHistone Deacetylase 3Histone Deacetylases

Identifiers

PMID21521655
PMCPMC3111848
OpenAlexW2043685018

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.