CoChat
Sign Up
Cited by 280Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeural dynamics and brain function

Altered Cortical Synaptic Morphology and Impaired Memory Consolidation in Forebrain- Specific Dominant-Negative PAK Transgenic Mice

Open access
Hayashi, Mansuo L, Choi, Se-Young, Rao, B.S.Shankaranarayana, Jung, Hae-Yoon, Lee, Hey-Kyoung, Zhang, Dawei, Chattarji, Sumantra, Kirkwood, Alfredo +1 more·2004·Neuron
DOI 10.1016/j.neuron.2004.05.003
Open this paper in CoChat — free accountOpen PDF

Abstract

Molecular and cellular mechanisms for memory consolidation in the cortex are poorly known. To study the relationships between synaptic structure and function in the cortex and consolidation of long-term memory, we have generated transgenic mice in which catalytic activity of PAK, a critical regulator of actin remodeling, is inhibited in the postnatal forebrain. Cortical neurons in these mice displayed fewer dendritic spines and an increased proportion of larger synapses compared to wild-type controls. These alterations in basal synaptic morphology correlated with enhanced mean synaptic strength and impaired bidirectional synaptic modifiability (enhanced LTP and reduced LTD) in the cortex. By contrast, spine morphology and synaptic plasticity were normal in the hippocampus of these mice. Importantly, these mice exhibited specific deficits in the consolidation phase of hippocampus-dependent memory. Thus, our results provide evidence for critical relationships between synaptic morphology and bidirectional modifiability of synaptic strength in the cortex and consolidation of long-term memory.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.neuron.2004.05.003

Cites

87 of 87 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Alterations in the regulation of actin at dendritic spines by neurodevelopmental disease-associated proteins such as DISC1, DTNBP1, SHANK3, PAK3, Oligophrenin and SRGAP2 produce deficits in synaptic plasticity and in the formation and consolidation of long-term memories.

    “Moreover, alterations in the regulation of actin at dendritic spines, by neurodevelopmental disease-associated proteins such as DISC1, DTNBP1, SHANK3, PAK3, Oligophrenin and SRGAP2, have been shown to produce deficits in both synaptic plasticity and the formation and consolidation of long-term memories.23, 24, 25, 26, 27, 28, 29”

    From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [26]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

  • CYFIP1 is part of a growing number of mental illness-associated actin-regulatory molecules, including DISC1, DTNBP1, SHANK3, SRGAP2, Oligophrenin and the Abi1-WAVE2 complex, that act in Rac1-dependent pathways to regulate dendritic development and spine dynamics.

    “Our results suggest that CYFIP1 is part of a growing number of mental illness-associated actin-regulatory molecules, including DISC1, DTNBP1, SHANK3, SRGAP2, Oligophrenin and the Abi1-WAVE2 complex that act in Rac1-dependent pathways to regulate dendritic development and spine dynamics.24, 25, 26, 27, 28, 29”

    From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [26]

    Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Hayashi, M. L., Choi, S.-Y., Rao, B. S. S., Jung, H.-Y., Lee, H.-K., Zhang, D., Chattarji, S., Kirkwood, A., & Tonegawa, S.
Affiliations
  • Howard Hughes Medical Institute (US)
  • Johns Hopkins University (US)
  • Tata Institute of Fundamental Research (IN)
Corresponding author
Tonegawa, Susumu
ORCID
Venue
Neuron
Publisher
Elsevier BV
Published
2004-06
Volume
42
Issue
5
Pages
773-787
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/j.neuron.2004.05.003
OpenAlex
W2006423839
Cited by
280
References
87
Citations by year
2026: 1 · 2025: 6 · 2024: 2 · 2023: 5 · 2022: 7 · 2021: 6 · 2020: 6 · 2019: 11 · 2018: 7 · 2017: 14 · 2016: 19 · 2015: 7 · 2014: 22 · 2013: 19 · 2012: 13
FWCI
6.93
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • Seoul National University Open Repository (Seoul National University) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
p21-activated kinase, dendritic spines, memory consolidation, long-term memory, synaptic plasticity, long-term potentiation, long-term depression, actin cytoskeleton remodeling, hippocampal-dependent memory
MeSH terms
Analysis of Variance, Animals, Animals, Newborn, Behavior, Animal, Dendrites, Drug Interactions, Enzyme Activation, Glycine, Hippocampus, Immunohistochemistry, Male, Memory Disorders, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Electron, Models, Neurological, Nerve Tissue Proteins, Neurons, Retention, Psychology, Spatial Behavior, Synapses, Time Factors, Valine, Blotting, Northern, Blotting, Western, Proto-Oncogene Proteins c-myc, Prosencephalon, Silver Staining, Synaptophysin, Neurofilament Proteins, Protein Serine-Threonine Kinases, In Situ Hybridization, Long-Term Potentiation, alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Maze Learning, Long-Term Synaptic Depression, Mice, Rats, p21-Activated Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review