The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index; 18 of the 28 sources its claims cite were checked for support.
Local, persistent activation of Rho GTPases during plasticity of single dendritic spines
Open accessAbstract
The Rho family of GTPases have important roles in the morphogenesis of the dendritic spines of neurons in the brain and synaptic plasticity by modulating the organization of the actin cytoskeleton. Here we used two-photon fluorescence lifetime imaging microscopy to monitor the activity of two Rho GTPases-RhoA and Cdc42-in single dendritic spines undergoing structural plasticity associated with long-term potentiation in CA1 pyramidal neurons in cultured slices of rat hippocampus. When long-term volume increase was induced in a single spine using two-photon glutamate uncaging, RhoA and Cdc42 were rapidly activated in the stimulated spine. These activities decayed over about five minutes, and were then followed by a phase of persistent activation lasting more than half an hour. Although active RhoA and Cdc42 were similarly mobile, their activity patterns were different. RhoA activation diffused out of the stimulated spine and spread over about 5 µm along the dendrite. In contrast, Cdc42 activation was restricted to the stimulated spine, and exhibited a steep gradient at the spine necks. Inhibition of the Rho-Rock pathway preferentially inhibited the initial spine growth, whereas the inhibition of the Cdc42-Pak pathway blocked the maintenance of sustained structural plasticity. RhoA and Cdc42 activation depended on Ca(2+)/calmodulin-dependent kinase (CaMKII). Thus, RhoA and Cdc42 relay transient CaMKII activation to synapse-specific, long-term signalling required for spine structural plasticity.
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Written from the paper’s full text.
TL;DR
Using 2pFLIM in single dendritic spines, this study shows that RhoA and Cdc42 are rapidly activated after glutamate uncaging, decay over ~5 min, and then remain active for more than 30 min during LTP-associated structural plasticity. RhoA activity spreads along dendrites, whereas Cdc42 activity stays spine-restricted, and the two GTPases support distinct phases of spine enlargement through Rho-Rock and Cdc42-Pak signaling downstream of CaMKII.
Key findings
- In stimulated spines, RhoA and Cdc42 activated within ~30 s, decayed over ~5 min, and showed persistent activity lasting more than 30 min; spine volume rose by ~300% transiently and relaxed to a sustained 70–80% increase for >30 min.
- RhoA activation spread into dendrites with a length constant of 4.5 μm and invaded ~25% of surrounding spines, while Cdc42 activation was restricted to the stimulated spine with a dendritic length constant of ~1.9 μm.
- AP5 abolished RhoA/Cdc42 activation and spine enlargement; KN62 and AIP2 inhibited activation more strongly in the sustained phase, indicating CaMKII dependence.
- Rho/Rock inhibition suppressed both transient and sustained volume changes, whereas Cdc42/Pak inhibition selectively decreased the sustained phase, suggesting distinct roles in spine structural plasticity.
Methods
- Cultured hippocampal slices from postnatal day 6–7 rats; CA1 pyramidal neurons were ballistically transfected with RhoA or Cdc42 FRET sensors at days in vitro 10–14 and imaged 2–4 days later.
- Rho GTPase activity was measured with 2-photon fluorescence lifetime imaging microscopy (2pFLIM), and spine volume was monitored from mCherry-RBD-mCherry fluorescence; structural plasticity was induced by 30 two-photon glutamate uncaging pulses at 0.5 Hz in zero extracellular Mg2+.
- Pharmacological inhibitors, shRNA knockdown, rescue constructs, and photoactivatable GFP diffusion measurements were used; most imaging was at room temperature (25–27°C), with similar results also obtained at 32–34°C.
Limitations
- The paper notes that shRNA-mediated protein downregulation is partial and requires relatively long expression (4 days), and that most imaging experiments were performed at room temperature, although near-physiological temperature gave similar results.
- Evident from the text: experiments use cultured hippocampal slices and sparse transfection/overexpression of FRET sensors, and conclusions from pharmacological inhibitors such as AP5, KN62, GH1152, and IPA3 may be limited by potential off-target effects.
- The paper does not include a dedicated limitations section beyond these points.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
18 of 28 cited sources checked · 9 supported · 0 flagged · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Thus, RhoA and Cdc42 relay transient CaMKII activation13 to synapse-specific, long-term signalling required for spine structural plasticity.”
- Also stated in: § Abstract · plain
“Localized, persistent activation of RhoA and Cdc42, which peaks in between CaMKII activation and the volume change (Fig. 4l), relays the transient CaMKII signalling13 to long-term spine structural plasticity (Fig. 4k).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) source
The citation is attached to “transient CaMKII activation,” not to the citing authors’ conclusion about RhoA and Cdc42. The paper’s “Mechanisms of spine specific CaMKII activation” section (page unavailable) reports that CaMKII activity decayed within seconds after stimulation, supporting the cited point. (LLM, conf=0.93)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: Long-lasting, spine-specific plasticity requires signalling pathways that relay compartmentalized signalling on the time scale of minutes to hours.
- Also stated in: § Abstract · plain
Every source the paper cites for this claim was checked and supports it.
In the paper
“The length constant of spread along the dendrite was 4.5 μm (Fig. 3a, b), a value similar to that for HRas (~10 μm)12.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [12] Harvey, C. D., Yasuda, R., Zhong, H. & Svoboda, K. The spread of Ras activity triggered by activation of a single dendritic spine. Science 321, 136–140 (2008) source
The citation is attached to the comparison with HRas (~10 μm), not to the citing paper’s 4.5 μm RhoA measurement. The source reports a Ras diffusion length constant of ~10 μm (p. 3), supporting the attributed comparison. (LLM, conf=0.94)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“When long-term volume increase was induced in a single spine using 2-photon glutamate uncaging14,15, RhoA and Cdc42 were rapidly activated in the stimulated spine.”
- Also stated in: § Abstract · plain
“When spine structural plasticity was induced, both RhoA (Fig. 1a, b) and Cdc42 (Fig. 2a, b) were activated rapidly within ~30 s in the stimulated spines.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) source
The Abstract describes two-photon glutamate uncaging at single spines and reports persistent enlargement of stimulated spines. The citation is attached to that experimental procedure, not to the subsequent statement about RhoA and Cdc42 activation. (LLM, conf=0.92)
- Supportedcites [15] Honkura, N., Matsuzaki, M., Noguchi, J., Ellis-Davies, G. C. & Kasai, H. The subspine organization of actin fibers regulates the structure and plasticity of dendritic spines. Neuron 57, 719–729 (2008) source
The citation is attached to the two-photon glutamate-uncaging method used to induce lasting enlargement of a single spine, not to the subsequent RhoA and Cdc42 result. The “Enlargement Pool of F-Actin in Dendritic Spines” section describes single-spine uncaging and reports long-term enlargement after the stimulus; the Experimental Procedures specify two-photon uncaging at 710 nm. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) sourceExperimental — accuracy not yet measured
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)
- Not checked yetcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) source
Checked before — its earlier verdict is held back until a new check runs.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: Long-lasting, spine-specific plasticity requires signalling pathways that relay compartmentalized signalling on the time scale of minutes to hours.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, Cdc42 activation was restricted to the stimulated spines (Fig. 3c, d), showing a spatial pattern similar to that of CaMKII13.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) source
The citation supports the comparison to CaMKII, not the citing paper’s observation about Cdc42. In ‘CaMKII activation during structural plasticity of dendritic spines’ (page not supplied), the source says CaMKII activity was restricted to stimulated spines and did not spread to dendrites or adjacent spines. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The difference between wild-type Rho GTPases and constitutively active mutants presumably reflects the difference in the fraction of the protein bound to the plasma membrane, as active Rho GTPases are localized on the plasma membrane21.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [21] Michaelson, D. et al. Differential localization of Rho GTPases in live cells: regulation by hypervariable regions and RhoGDI binding. J. Cell Biol. 152, 111–126 (2001) sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that Dbl-stimulated Rho GTPases associated predominantly with plasma-membrane regions. But it also states that constitutively active mutants localized to both the plasma membrane and internal membranes, so the claim overstates plasma-membrane localization as a general rule for active Rho GTPases. (LLM, conf=0.88)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Under the basal condition, there was no correlation between the activity of Rho GTPases and spine volume (Supplementary Fig. 4).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A small fraction of Cdc42 activation spread into the dendrite and decayed sharply with a length constant of ~1.9 μm (Fig. 3c, d).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“RhoA activation diffused out of the stimulated spine and spread over ~5 μm along the dendrite.”
- Also stated in: § Abstract · plain
“RhoA activation spread into the dendrites over several micrometers (Fig. 1a–c, 3a, b), and slightly invaded surrounding spines (~25% of the stimulated spines).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Abstract · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although active RhoA and Cdc42 were similarly mobile, their activity patterns were different.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- Probably not a substantial claim. 2
- It may state two separate claims as one. 22
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Amongst known effectors of Rho and Cdc42, Rock and Pak are two kinases that can be activated repsectively by these GTPases24–26.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Not checked — no full text of the sourcecites [24] Nikolić, M. The Pak1 kinase: an important regulator of neuronal morphology and function in the developing forebrain. Mol. Neurobiol. 37, 187–202 (2008) source
- Partly supportedcites [25] Kreis, P. et al. The p21-activated kinase 3 implicated in mental retardation regulates spine morphogenesis through a Cdc42-dependent pathway. J. Biol. Chem. 282, 21497–21506 (2007) sourceExperimental — accuracy not yet measured
The section “R67C Mutation Impairs Kinase Activation by Cdc42” reports that PAK3 is activated by the intersectin–Cdc42 module, supporting the Pak–Cdc42 part of the claim. The passages found in our copy do not establish that ROCK is activated by Rho (searched: “ROCK” and “ROCK Rho kinase activated by Rho”). (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [26] Iden, S. & Collard, J. G. Crosstalk between small GTPases and polarity proteins in cell polarization. Nature Rev. Mol. Cell Biol. 9, 846–859 (2008) source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These values are ~10 times larger than the decay time constant of cytosolic paGFP (~0.4 s) and similar to that of a constitutively active HRas mutant (~6 s) (Fig. 3e–h)12.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [12] Harvey, C. D., Yasuda, R., Zhong, H. & Svoboda, K. The spread of Ras activity triggered by activation of a single dendritic spine. Science 321, 136–140 (2008) sourceExperimental — accuracy not yet measured
The mobility results (p. 2) report that paGFP-Ras decayed more than ten times slower than cytosolic paGFP and that constitutively active Ras G12V diffused similarly to wild-type Ras. Figure 3B’s caption (p. 8) identifies the cytosolic and Ras G12V comparisons, but our copy does not give the cited numerical estimates of ~0.4 s and ~6 s. The Rho GTPase values appear to be the citing authors’ own results, not a finding attributed to this source. (LLM, conf=0.83)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, HRas activity spreads from the stimulated spines along dendrites and into surrounding spines over ~10 μm12.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [12] Harvey, C. D., Yasuda, R., Zhong, H. & Svoboda, K. The spread of Ras activity triggered by activation of a single dendritic spine. Science 321, 136–140 (2008) source
The Abstract (p. 1) identifies H-Ras as the signaling molecule studied and reports that Ras activity spread approximately 10 micrometers along the dendrite and invaded neighboring spines. The spatial-profile passage (p. 2) likewise reports spread along the parent dendrite into nearby spines. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CaMKII activation is restricted to spines, and decays rapidly with a time constant of ~10 s13.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) sourceExperimental — accuracy not yet measured
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)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) sourceExperimental — accuracy not yet measured
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)
- Not checked yetcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) source
Checked before — its earlier verdict is held back until a new check runs.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, inhibition of Pak with IPA3 (100 μM)28 decreased the sustained volume change selectively without changing the transient volume change (Fig. 4h, i, j) similarly to inhibition of Cdc42 signalling (Fig. 4e, g).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [28] Deacon, S. W. et al. An isoform-selective, small-molecule inhibitor targets the autoregulatory mechanism of p21-activated kinase. Chem. Biol. 15, 322–331 (2008) source
The citation identifies IPA-3 as a Pak inhibitor. The source’s “IPA-3 Is a Direct, Noncompetitive Inhibitor of Pak1” section reports that IPA-3 prevents Pak1 activation; the sustained and transient volume changes are results attributed to the citing paper’s own Figure 4, not to this source. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Partly supportedcites [12] Harvey, C. D., Yasuda, R., Zhong, H. & Svoboda, K. The spread of Ras activity triggered by activation of a single dendritic spine. Science 321, 136–140 (2008) sourceExperimental — accuracy not yet measured
The paper reports that glutamate uncaging caused sustained enlargement of the stimulated spine (p. 1). Its Figure 1 caption (p. 6) describes spine-volume measurements, but the text does not give a rapid ~300% increase or a sustained 70–80% increase for more than 30 minutes; it defines the sustained measurement at 15.5–19.5 minutes. (LLM, conf=0.86)
- Partly supportedcites [13] Lee, S. J., Escobedo-Lozoya, Y., Szatmari, E. M. & Yasuda, R. Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458, 299–304 (2009) sourceExperimental — accuracy not yet measured
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)
- Partly supportedcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) sourceExperimental — accuracy not yet measured
The passage labeled Abstract reports rapid spine enlargement after glutamate uncaging and enlargement lasting 70–100 minutes in 30% of stimulated spines. It gives a mean maximal volume increase of 203 ± 37%, not approximately 300%, and reports persistent increases greater than 50%, not a sustained level of 70–80%. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Rho GTPases may constitute such signalling, because they play important roles in regulating actin cytoskeleton3,16, which is essential for spine-specific, long-term structural and functional plasticity14,17.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [3] Saneyoshi, T., Fortin, D. A. & Soderling, T. R. Regulation of spine and synapse formation by activity-dependent intracellular signaling pathways. Curr. Opin. Neurobiol. 20, 108–115 (2009) source
The “Regulation of spine and synapse formation by small GTPases” section says that small GTPases largely regulate the actin cytoskeleton that modulates spine morphology and synapse function. The “Future directions” section likewise describes these pathways as major players in spine morphology. The sentence attaches this source’s citation to the actin-regulation clause, not the separate long-term-plasticity clause. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [16] Heasman, S. J. & Ridley, A. J. Mammalian Rho GTPases: new insights into their functions from in vivo studies. Nature Rev. Mol. Cell Biol. 9, 690–701 (2008) source
- Not checked yetcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked — no full text of the sourcecites [17] Okamoto, K., Nagai, T., Miyawaki, A. & Hayashi, Y. Rapid and persistent modulation of actin dynamics regulates postsynaptic reorganization underlying bidirectional plasticity. Nature Neurosci. 7, 1104–1112 (2004) source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The short length constant of Cdc42 in the dendrites (1.9 μm, Fig. 3) also supports the fast inactivation of Cdc42 in the dendrite: the inactivation time constant τ is related to the length constant L and the diffusion constant D~0.6 μm2 (Ref 12) as τ = L2/D, and thus is ~6 s for Cdc42 and ~30 s for RhoA, compared to 200–300 s for HRas12.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Supportedcites [12] Harvey, C. D., Yasuda, R., Zhong, H. & Svoboda, K. The spread of Ras activity triggered by activation of a single dendritic spine. Science 321, 136–140 (2008) source
The cited paper identifies its Ras indicator as containing HRas (p. 1). It reports an inactivation time constant of 4.5 ± 0.4 minutes (about 270 seconds) and a diffusion coefficient of 0.65 μm²/s (p. 3), matching the approximate HRas values attributed to it. The 6-second Cdc42 and 30-second RhoA figures are calculations made by the citing authors, not findings attributed to this source. (LLM, conf=0.91)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, Cdc42 activation was restricted to the stimulated spine, and exhibited a steep gradient at the spine necks.”
- Also stated in: § Abstract · plain
“In contrast, Cdc42 activation was restricted to the stimulated spines (Fig. 2a–c, 3c, d).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Abstract · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These activities decayed over ~5 min, and were then followed by a phase of persistent activation lasting more than 30 min.”
- Also stated in: § Abstract · plain
“The activation decayed over ~5 min, followed by sustained activity lasting more than 30 min.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Abstract · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, shRNA against Cdc42 decreased the sustained volume change, but not the transient volume change (Fig. 4e, i, j).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Downregulation of RhoA and RhoB with short-hairpin RNA (shRNA) decreased the transient volume change, but did not appreciably affect the sustained volume change (Fig. 4a, i, j).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Inhibition of the Rho-Rock pathway preferentially inhibited the initial spine growth, whereas the inhibition of the Cdc42-Pak pathway blocked the maintenance of sustained structural plasticity.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There was only a small fraction (10–20 %) of fluorescence remaining at 20 s after photoactivation (Fig. 3e–h), suggesting that no major immobile fraction of RhoA or Cdc42 exists in spines.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The phenotypes caused by these shRNAs were rescued by co-expressing shRNA-resistant mEGFP-Rho GTPases (Fig. 4b, f, i, j), indicating that the effect of the shRNAs are specific and the mEGFP-RhoA and mEGFP-Cdc42 used in the FRET sensors are functional as endogenous proteins.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, our data suggest that Rho signalling is required for the transient phase and likely the sustained phase of spine enlargement, while Cdc42 signalling is required for the sustained phase.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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In the paper
“The time course of spine enlargement in neurons expressing the FRET sensor was similar to that in neurons expressing only EGFP (Fig. 4)14, suggesting that the overexpression of FRET sensors causes almost no effects on spine structural plasticity (Supplementary note).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
What the sources say
- Not checked yetcites [14] Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. & Kasai, H. Structural basis of long-term potentiation in single dendritic spines. Nature 429, 761–766 (2004) source
Checked before — its earlier verdict is held back until a new check runs.
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In the paper
“These sensors were verified to be specific and sensitive under 2pFLIM (Supplementary note).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together with the results from Rho/Cdc42 inhibition (Fig. 4a–j), our data implies that the Rho-Rock pathway is required for both transient and sustained phase, while the Cdc42-Pak pathway is required for the sustained phase of the structural plasticity but not for the transient phase (Fig. 4k).”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Since the high spatial gradient of Cdc42 between the stimulated spines and dendrite was maintained for more than 20–30 min (Fig. 2b, c, 3d), Cdc42 must be continuously activated at the stimulated spines during plasticity, and inactivated immediately after diffusing out of the spines.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, Cdc42 is as mobile as RhoA and HRas, yet only Cdc42 shows the compartmentalized activity.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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In the paper
“Neither C3 nor Wasp affected CaMKII activation (Supplementary Fig. 9), indicating that there is no feedback signalling from Rho and Cdc42 to upstream Ca2+ and CaMKII.”
§ Local, persistent activation of Rho GTPases during plasticity of single dendritic spines > Abstract
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The paper relies on this without support.
Long-lasting, spine-specific plasticity requires signalling pathways that relay compartmentalized signalling on the time scale of minutes to hours.
“However, in order to achieve long-lasting, spine-specific plasticity, there should also exist signalling pathways that relay compartmentalized signalling in the time scale of minutes to hours.”
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Also the diffusion kinetics of both molecules were comparable and similar to Ras diffusion and showed no immobile fraction left in the spine.”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Ras activity was shown to invade typically 10–20 neighboring spines in a range of 10 μm along the dendrite, whereas RhoA activity only spread 5 μm and rarely invaded neighboring spines (Harvey et al., 2008; Murakoshi et al., 2011).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Nevertheless, Cdc42 activity remained spatially confined, because it had an intrinsic inactivation time constant of 6 s and therefore depends on continuous activation by CaMKII (Murakoshi et al., 2011).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Indeed, there is compelling evidence that CaMKII, via phosphorylation, initiates a series of actin-based cytoskeletal rearrangements in the spine (32, 312–314).”
From Synaptic memory and CaMKII (2023) · cites this paper as [312]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Indeed spine growth is likely to be a multifaceted event involving regulated changes in cytoskeletal elements, membrane addition, and receptor trafficking under the control of multiple small GTPases”
From Ral mediates activity‐dependent growth of postsynaptic membranes via recruitment of the exocyst (2013) · cites this paper as Murakoshi et al, 2011
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“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 Murakoshi et al., 2011
The cited source says what the claim attributes to it.
In the citing paper
“In contrast, Rho inactivated five times slower and could therefore spread into the dendrite.”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
The cited source says what the claim attributes to it.
In the citing paper
“Both Cdc42 and Rho showed a rapid activity peak 30 s after stimulation followed by decay over 5 min and a sustained lower activity for more than 30 min.”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
The cited source says what the claim attributes to it.
In the citing paper
“CaMKII-Cdc42-Pak signaling increases spine volume and synaptic strength (Murakoshi et al., 2011)”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Murakoshi et al., 2011
The cited source says what the claim attributes to it.
In the citing paper
“and that the Rho GTPases Cdc42 and RhoA are required for LTP and sLTP (312, 313).”
From Synaptic memory and CaMKII (2023) · cites this paper as [312]
In the citing paper
“The mechanism underlying this phenomenon involves local spreading of signaling cascades from the activated spine to its neighbors, and some of these spreading signals are potent drivers of F-actin dynamics (24–26).”
From Synaptic evidence for the efficacy of spaced learning (2012) · cites this paper as [24]
In the citing paper
“This form of plasticity shares many properties with Schaffer collateral LTP, including dependence on N-methyl-d-aspartate receptors (NMDARs), Rho GTPase signaling, Ca2+/calmodulin-dependent protein kinase II (CaMKII) phosphorylation, F-actin polymerization and synaptic AMPAR insertion (20–24).”
From Synaptic evidence for the efficacy of spaced learning (2012) · cites this paper as [24]
In the citing paper
“Prior work suggesting that strong stimulation of single synapses causes the spread of active GTPases to neighboring spines (24, 25) is of interest in this regard because these enzymes play critical roles in the production of stable LTP.”
From Synaptic evidence for the efficacy of spaced learning (2012) · cites this paper as [24]
In the citing paper
“because these enzymes play critical roles in the production of stable LTP.”
From Synaptic evidence for the efficacy of spaced learning (2012) · cites this paper as [24]
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Metadata
- Authors
- Murakoshi, H., Wang, H., & Yasuda, R.
- Affiliations
- Duke Medical Center (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Yasuda, Ryohei
- Venue
- Nature
- Published
- 2011-03-20
- Volume
- 472
- Issue
- 7341
- Pages
- 100-104
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3105377
- OpenAlex
- W2092348167
- Semantic Scholar
- 68ac950b74f2a3fe5c7522a7290439c9214f5f35
- Cited by
- 564
- References
- 43
- Citations by year
- 2026: 16 · 2025: 26 · 2024: 25 · 2023: 32 · 2022: 42 · 2021: 48 · 2020: 34 · 2019: 34 · 2018: 35 · 2017: 41 · 2016: 58 · 2015: 39 · 2014: 48 · 2013: 37 · 2012: 32
- FWCI
- 17.75
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- National Institute of Mental Health (R01MH080047)
- National Institute on Drug Abuse (R01DA027807)
- National Institute of Neurological Disorders and Stroke (R01NS068410)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- dendritic spines, Rho GTPases, RhoA, Cdc42, long-term potentiation, synaptic plasticity, CaMKII, spine morphogenesis, actin cytoskeleton, CA1 pyramidal neurons, hippocampus, glutamate uncaging, fluorescence lifetime imaging, learning and memory
- MeSH terms
- Animals, Enzyme Activation, Humans, Learning, Microscopy, Fluorescence, Neuronal Plasticity, Phosphoproteins, Time Factors, Signal Transduction, Long-Term Potentiation, Pyramidal Cells, GTPase-Activating Proteins, rho GTP-Binding Proteins, rhoA GTP-Binding Protein, Dendritic Spines, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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