Cited by 1,025Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsTreatment of Major Depression

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Shrinkage of Dendritic Spines Associated with Long-Term Depression of Hippocampal Synapses

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Zhou, Qiang, Homma, Koichi J., Poo, Mu-ming·2004·Neuron

DOI 10.1016/j.neuron.2004.11.011

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Abstract

Activity-induced modification of neuronal connections is essential for the development of the nervous system and may also underlie learning and memory functions of mature brain. Previous studies have shown an increase in dendritic spine density and/or enlargement of spines after the induction of long-term potentiation (LTP). Using two-photon time-lapse imaging of dendritic spines in acute hippocampal slices from neonatal rats, we found that the induction of long-term depression (LTD) by low-frequency stimulation is accompanied by a marked shrinkage of spines, which can be reversed by subsequent high-frequency stimulation that induces LTP. The spine shrinkage requires activation of NMDA receptors and calcineurin, similar to that for LTD. However, spine shrinkage is mediated by cofilin, but not by protein phosphatase 1 (PP1), which is essential for LTD, suggesting that different downstream pathways are involved in spine shrinkage and LTD. This activity-induced spine shrinkage may contribute to activity-dependent elimination of synaptic connections.

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Authors: Zhou, Q., Homma, K. J., & Poo, M.-M.
Affiliations: University of California, Berkeley (US)
Corresponding author: Poo, Mu-ming
ORCID: Zhou, Qiang
Homma, Koichi J.
Poo, Mu-ming
Venue: Neuron
Publisher: Elsevier BV
Published: 2004-12
Volume: 44
Issue: 5
Pages: 749-757
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/j.neuron.2004.11.011
OpenAlex: W2107611011
Cited by: 1,025
References: 56
Citations by year: 2026: 17 · 2025: 30 · 2024: 29 · 2023: 24 · 2022: 35 · 2021: 49 · 2020: 55 · 2019: 45 · 2018: 55 · 2017: 43 · 2016: 44 · 2015: 54 · 2014: 64 · 2013: 54 · 2012: 58
FWCI: 14.56
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3150 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Neuron (publishedVersion)
PubMed (publishedVersion)
Institutional Repositories DataBase (IRDB) (submittedVersion)
Funders: National Institutes of Health
National Institute of Neurological Disorders and Stroke (NS37831, R01NS036999, NS 36999, R01NS037831)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Keywords: long-term depression, long-term potentiation, hippocampal synapses, NMDA receptor, calcineurin, cofilin, protein phosphatase 1, synaptic plasticity, low-frequency stimulation, high-frequency stimulation
MeSH terms: Animals, Electrophysiology, Hippocampus, Microfilament Proteins, Synapses, Signal Transduction, Rats, Sprague-Dawley, Long-Term Synaptic Depression, Dendritic Spines, Actin Depolymerizing Factors, Rats, In Vitro Techniques

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Shrinkage of Dendritic Spines Associated with Long-Term Depression of Hippocampal Synapses

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