Optical induction of plasticity at single synapses reveals input-specific accumulation of αCaMKII
Open accessAbstract
Long-term potentiation (LTP), a form of synaptic plasticity, is a primary experimental model for understanding learning and memory formation. Here, we use light-activated channelrhodopsin-2 (ChR2) as a tool to study the molecular events that occur in dendritic spines of CA1 pyramidal cells during LTP induction. Two-photon uncaging of MNI-glutamate allowed us to selectively activate excitatory synapses on optically identified spines while ChR2 provided independent control of postsynaptic depolarization by blue light. Pairing of these optical stimuli induced lasting increase of spine volume and triggered translocation of alphaCaMKII to the stimulated spines. No changes in alphaCaMKII concentration or cytoplasmic volume were observed in neighboring spines on the same dendrite, providing evidence that alphaCaMKII accumulation at postsynaptic sites is a synapse-specific memory trace of coincident activity.
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The input specificity of LTP is generated by the input-specific accumulation of CaMKII.
“which helps explain how the input specificity of LTP (i.e., the fact that LTP is induced only at the stimulated synapse and not at its neighbors) is generated by the input-specific accumulation of CaMKII.34”
From LTP expression mediated by autonomous activity of GluN2B-bound CaMKII (2024) · cites this paper as [34]
The Abstract proposes that αCaMKII accumulation could account for the synapse-specificity of LTP, and the Discussion reports increased αCaMKII in spines with lasting changes but not, on average, in unstimulated neighbors. The paper supports input-specific accumulation, but does not establish that this accumulation generates LTP’s input specificity. Page numbers are unavailable in our copy. (LLM, conf=0.88)
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Cites
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- Authors
- Zhang, Y.-P., Holbro, N., & Oertner, T. G.
- Affiliations
- Friedrich Miescher Institute, Maulbeerstrasse 66, CH-4058 Basel, Switzerland
- Johns Hopkins University (US)
- Corresponding author
- Oertner, Thomas G.
- ORCID
- Oertner, Thomas G.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2008-08-19
- Volume
- 105
- Issue
- 33
- Pages
- 12039-12044
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2575337
- OpenAlex
- W2146033515
- Cited by
- 140
- References
- 7
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 7 · 2021: 4 · 2020: 5 · 2019: 10 · 2018: 1 · 2017: 5 · 2016: 3 · 2015: 6 · 2014: 16 · 2013: 6 · 2012: 15
- FWCI
- 7.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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 › Treatment of Major Depression
- Keywords
- long-term potentiation, synaptic plasticity, CaMKIIα, channelrhodopsin-2, optogenetics, two-photon uncaging, dendritic spines, CA1 pyramidal neurons, memory traces, learning and memory
- MeSH terms
- Animals, Color, Light, Synapses, Visual Perception, Rats, Wistar, Glutamic Acid, Protein Subunits, Dendritic Spines, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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