Activation of CaMKII in single dendritic spines during long-term potentiation
Open accessAbstract
Calcium/calmodulin-dependent kinase II (CaMKII) plays a central part in long-term potentiation (LTP), which underlies some forms of learning and memory. Here we monitored the spatiotemporal dynamics of CaMKII activation in individual dendritic spines during LTP using two-photon fluorescence lifetime imaging microscopy, in combination with two-photon glutamate uncaging. Induction of LTP and associated spine enlargement in single spines triggered transient ( approximately 1 min) CaMKII activation restricted to the stimulated spines. CaMKII in spines was specifically activated by NMDA receptors and L-type voltage-sensitive calcium channels, presumably by nanodomain Ca(2+) near the channels, in response to glutamate uncaging and depolarization, respectively. The high degree of compartmentalization and channel specificity of CaMKII signalling allow stimuli-specific spatiotemporal patterns of CaMKII signalling and may be important for synapse-specificity of synaptic plasticity.
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Spine CaMKII activity as monitored with FRET imaging during LTP only remained elevated for ∼1 min after the induction of LTP, suggesting that conformational changes associated with CaMKII activation due to either Ca2+/CaM or autophosphorylation are transient.
“Second, spine CaMKII activity as monitored with fluorescence resonance energy transfer (FRET) imaging (188) during LTP only remained elevated for ∼1 min after the induction of LTP, suggesting that conformational changes associated with CaMKII activation due to either Ca2+/CaM or autophosphorylation are transient.”
From Synaptic memory and CaMKII (2023) · cites this paper as [188]
Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable, 1 not checked. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe NMDA receptor-CaMKII-Cdc42-Pak pathway constitutes the spine-specific signal transduction spanning the time scale from sub-second to more than 30 min to cause sustained structural and functional spine plasticity.
“the NMDA receptor-CaMKII-Cdc42-Pak pathway (red line in Fig. 4k) constitutes the spine specific signal transduction spanning the time scale from sub-second to more than 30 min to cause sustained structural and functional spine plasticity”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
The section ‘CaMKII activation during structural plasticity of dendritic spines’ (page unavailable) reports NMDA-receptor-dependent, spine-restricted CaMKII activation and spine enlargement lasting more than 30 minutes. It does not establish a Cdc42–Pak pathway, a sub-second-to-30-minute signaling cascade, or that this pathway causes sustained functional as well as structural plasticity. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCaMKII activation is restricted to spines and decays rapidly with a time constant of ~10 s.
“CaMKII activation is restricted to spines, and decays rapidly with a time constant of ~10 s13.”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
The Discussion says CaMKII activation is largely restricted to the stimulated spine during LTP. However, the Mechanisms of spine specific CaMKII activation section reports two inactivation time constants, 6 and 45 s, rather than a single time constant of approximately 10 s. The claim captures rapid, spine-specific activation but oversimplifies its decay kinetics. (LLM, conf=0.88)
Experimental — accuracy not yet measuredC3 and Wasp inhibited synaptic potentiation induced by pairing postsynaptic depolarization (0 mV) and 2-photon glutamate uncaging, suggesting Rho and Cdc42 are important for functional plasticity as well as structural plasticity of spines.
“C3 and Wasp also inhibited synaptic potentiation induced by pairing postsynaptic depolarization (0 mV) and 2-photon glutamate uncaging (Supplementary Fig. 10)13,14, suggesting that Rho and Cdc42 are important for the functional plasticity as well as the structural plasticity of spines.”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
The section “CaMKII activation during pairing-induced LTP” (page unavailable) reports synaptic potentiation induced by pairing 0 mV postsynaptic depolarization with two-photon glutamate uncaging. Our copy does not report that C3 or Wasp inhibited this potentiation, or draw the claimed conclusion about Rho and Cdc42. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe spine volume increased rapidly by ~300% following glutamate uncaging (transient phase) and relaxed to an elevated level of 70-80% for more than 30 min (sustained phase).
“The spine volume increased rapidly by ~300% following glutamate uncaging (transient phase) and relaxed to an elevated level of 70–80% for more than 30 min (sustained phase) (Figs. 1d, 2d)12–14.”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
The section “CaMKII activation during structural plasticity of dendritic spines” (page not provided) supports a rapid increase after glutamate uncaging followed by enlargement lasting more than 30 minutes. It reports 376 ± 68% initially and 104 ± 21% afterward, rather than the claimed ~300% and 70–80%. (LLM, conf=0.88)
Experimental — accuracy not yet measured
The diffusional coupling of CaMKII with the dendrite was significantly slower, in the range of several minutes.
“The diffusional coupling of CaMKII with the dendrite was significantly slower, in the range of several minutes (Lee et al., 2009),”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Lee et al., 2009
Upon single-spine glutamate uncaging, the activation of CaMKII peaked within 6 s and only lasted for a few minutes.
“Upon single-spine glutamate uncaging, the activation of CaMKII peaked within 6 s and only lasted for a few minutes (Lee et al., 2009).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Lee et al., 2009
This combination of techniques allowed recording activity patterns for CaMKII, Ras, RhoA and Cdc42 in dendritic spines following local glutamate uncaging.
“This combination of techniques allowed recording activity patterns for CaMKII (Lee et al., 2009), Ras (Harvey et al., 2008), RhoA and Cdc42 (Murakoshi et al., 2011) in dendritic spines following local glutamate uncaging.”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Lee et al., 2009
Activating VDCCs, which are present in spines, evokes cytosolic spine Ca2+ transients and the activation of cytosolic spine CaMKII.
“Activating VDCCs, which are present in spines, evokes cytosolic spine Ca2+ transients (185–187) and the activation of cytosolic spine CaMKII (188).”
From Synaptic memory and CaMKII (2023) · cites this paper as [188]
RhoA and Cdc42 relay transient CaMKII activation to synapse-specific, long-term signalling required for spine structural plasticity.
“Thus, RhoA and Cdc42 relay transient CaMKII activation13 to synapse-specific, long-term signalling required for spine structural plasticity.”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
Cdc42 activation showed a spatial pattern similar to that of CaMKII.
“In contrast, Cdc42 activation was restricted to the stimulated spines (Fig. 3c, d), showing a spatial pattern similar to that of CaMKII13.”
From Local, persistent activation of Rho GTPases during plasticity of single dendritic spines (2011) · cites this paper as [13]
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Oda, S., Tsuneoka, Y., Yoshida, S., Adachi‐Akahane, S., Ito, M., Kuroda, M., & Funato, H. (2018) · Journal of Comparative Neurology · doi:10.1002/cne.24409 · Cited by 27 · see citing works
- Authors
- Lee, S.-J. R., Escobedo-Lozoya, Y., Szatmari, E. M., & Yasuda, R.
- Affiliations
- Duke Medical Center (US)
- Corresponding author
- Yasuda, Ryohei
- Venue
- Nature
- Published
- 2009-03
- Volume
- 458
- Issue
- 7236
- Pages
- 299-304
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2719773
- OpenAlex
- W2046033738
- Cited by
- 685
- References
- 8
- Citations by year
- 2026: 16 · 2025: 35 · 2024: 31 · 2023: 32 · 2022: 32 · 2021: 36 · 2020: 28 · 2019: 40 · 2018: 38 · 2017: 37 · 2016: 45 · 2015: 49 · 2014: 53 · 2013: 53 · 2012: 40
- FWCI
- 22.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Autism Speaks (AS1398)
- National Institute of Mental Health (R01MH08004, R01MH080047)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- CaMKII, long-term potentiation, dendritic spines, NMDA receptor, L-type calcium channels, calcium signaling, synaptic plasticity, glutamate uncaging, fluorescence lifetime imaging
- MeSH terms
- Animals, Calcium, Cell Line, Cells, Cultured, Chelating Agents, Enzyme Activation, Fluorescence, Hippocampus, Humans, Kinetics, Synapses, Time Factors, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Photons, Glutamic Acid, Calcium Channels, L-Type, Fluorescence Resonance Energy Transfer, Dendritic Spines, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Synaptic Potentials
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