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Shrinkage of Dendritic Spines Associated with Long-Term Depression of Hippocampal Synapses
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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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“Conversely, the triggering of LTD is associated with the shrinkage of dendritic spines and perhaps even their disappearance (Na ¨gerl et al. 2004;Zhou et al. 2004;Wang et al. 2007;Kasai et al. 2010).”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Zhou et al. 2004
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“In contrast, when two cells co-activate infrequently, dendritic spines shrink or disappear, and the synaptic connection weakens and is likely to be eliminated.(64, 65)”
From Neglect as a violation of species-expectant experience: neurodevelopmental consequences (2017) · cites this paper as [64]
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Metadata
- Authors
- Zhou, Q., Homma, K. J., & Poo, M.-M.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Poo, Mu-ming
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 44
- Issue
- 5
- Pages
- 749-757
- ISSN
- 0896-6273 (ISSN-L)
- 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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