Activation of CaMKII in single dendritic spines during long-term potentiation

By Seok-Jin R. Lee, Yasmin Escobedo-Lozoya, E. Szatmari, R. Yasuda. Nature, 2009

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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 (∼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 Ca2+ 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.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7da24a1b5fea9a2615d402b9f461b4c6991dcafe

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Citations in the corpus

Heterosynaptic structural plasticity on local dendritic segments of hippocampal CA1 neurons (2014, background): “Inhibition of CaMKII blocks LTP and long-lasting spine enlargement (Lee et al., 2009; Matsuzaki et al., 2004).”
Mechanisms of CaMKII action in long-term potentiation (2012, methodology): “High-resolution imaging of CaMKII activation during LTP induction has been made possible by the development of the Camui activity senso”
Actin in dendritic spines: connecting dynamics to function (2010, background): “Monitoring the spatiotemporal dynamics of postsynaptic signals (Lee et al., 2009) and photoactivation localization microscopy (PALM)–based singlemolecule tracking to analyze cytoskeletal structures in single dendritic spines (Tatavarty et al., 2009) will be of great additional value.”
Synaptic Consolidation: From Synapses to Behavioral Modeling (2015, background): “…2011) which are not directly visible in electrophysiological experiments but must be inferred indirectly by pharmacological (Lisman et al., 2002; Sajikumar and Frey, 2004a; Ramachandran and Frey, 2009; Redondo et al., 2010) or spine imaging experiments (Lee et al., 2009; Okamoto et al., 2009).”
A Guide to Fluorescent Protein FRET Pairs (2016, background): “With the development of two-photon FLIM (2pFLIM), FRET imaging has been extended from cultured cells to living animals [118].”
Synaptic Plasticity Forms and Functions. (2020, background): “…of individual or small groups of synapses alone, without any correlated AP output, is adequate to generate an NMDAR-mediated Ca 2 + entry that,in turn,could activate a biochemical signaling molecule functioning as an ET (e.g., CaMKII) (Lee et al. 2009, Yagishita et al. 2014) ( Figure 5 b ).”
Structural and molecular remodeling of dendritic spine substructures during long-term potentiation (2014, positive): “To visualize the interaction between cofilin and actin, we employed Förster resonance energy transfer-fluorescent lifetime imaging (FRET-FLIM; Lee et al., 2009; Murakoshi et al., 2011) between donor cofilin-GFP and acceptor mRFP-actin (Figures 5A–5F).”
How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory (2019, background): “Because this hypothesis requires persistently active CaMKII, in the PSD and possibly below the resolution of earlier microscopy (Lee et al. 2009), further experiments to search for a persistent active CaMKII / NMDAR complex, perhaps using a FRET construct, would be desirable.”
Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, neutral): “Classic LTP in the CA1 region of the hippocampus is formally defined as input-specific homosynaptic facilitation(27,164,384) and is dependent on NMDAR activation, Ca(21) influx, and activation of Ca(21)dependent intracellular signaling pathways, notably the CaMKII pathway.(164) Although the increase”
COORDINATION OF SIZE AND NUMBER OF EXCITATORY AND INHIBITORY SYNAPSES RESULTS IN A BALANCED STRUCTURAL PLASTICITY ALONG MATURE HIPPOCAMPAL CA1 DENDRITES DURING LTP (2011, background): “TBS also elevates intracellular calcium from multiple sources and releases BDNF; events not elicited with tetanic stimulation (Larson et al., 1986; Abraham and Huggett, 1997; Kang et al., 1997;”
The dendritic branch is the preferred integrative unit for protein synthesis-dependent LTP (2011, methodology): “In agreement with previous studies (Harvey and Svoboda, 2007; Harvey et al., 2008; Honkura et al., 2008; Lee et al., 2009; Matsuzaki et al., 2004; Yasuda et al., 2006), we found that GLU stimulation (somatic potential change in response to uncaging pulse shown in S1G) resulted in E-LTP induction, na”
AMPARs and synaptic plasticity: the last 25 years. (2013, neutral): “The activation of CaMKII during LTP induction is only transient, returning to baseline within a few minutes (Lee et al., 2009).”
Learning rules and persistence of dendritic spines (2010, background): “In fact, CaMKII is also confined within the spine during enlargement (Lee et al., 2009).”