Kinetics of Endogenous CaMKII Required for Synaptic Plasticity Revealed by Optogenetic Kinase Inhibitor

Murakoshi, Hideji; Shin, Myung Eun; Parra-Bueno, Paula; Szatmári, E; Shibata, Akihiro; Yasuda, Ryohei

doi:10.1016/j.neuron.2017.04.027

Cited by 26 publications

(32 citation statements)

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“…Similarly, CaMKII is found to be necessary for the formation, but not for the maintenance or retrieval, of amygdala-dependent fear memory (Buard et al, 2010). More recent study with optogenetic inhibitor of CaMKII further refined the temporal window of CaMKII action (Murakoshi et al, 2017). This study showed that CaMKII activation is necessary only for the first ~1 min of LTP induction.…”

Section: Transient Ca2+ Elevation: the Trigger Of Multiple Signaling mentioning

confidence: 99%

“…This study showed that CaMKII activation is necessary only for the first ~1 min of LTP induction. In addition, CaMKII activation in amygdala during the training (~3 min), but not after the training, is required for fear memory formation in the inhibitory avoidance task (Murakoshi et al, 2017). This apparent inconsistency between the early biochemical studies and the results from pharmacological and optogenetic inhibition could be because autophosphorylation does not correlate with CaMKII activation under some conditions (Lengyel et al, 2004).…”

Section: Transient Ca2+ Elevation: the Trigger Of Multiple Signaling mentioning

confidence: 99%

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Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization

Nakahata

Yasuda

2018

Front. Synaptic Neurosci.

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177

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Dendritic spines are small protrusive structures on dendritic surfaces, and function as postsynaptic compartments for excitatory synapses. Plasticity of spine structure is associated with many forms of long-term neuronal plasticity, learning and memory. Inside these small dendritic compartments, biochemical states and protein-protein interactions are dynamically modulated by synaptic activity, leading to the regulation of protein synthesis and reorganization of cytoskeletal architecture. This in turn causes plasticity of structure and function of the spine. Technical advances in monitoring molecular behaviors in single dendritic spines have revealed that each signaling pathway is differently regulated across multiple spatiotemporal domains. The spatial pattern of signaling activity expands from a single spine to the nearby dendritic area, dendritic branch and the nucleus, regulating different cellular events at each spatial scale. Temporally, biochemical events are typically triggered by short Ca2+ pulses (~10–100 ms). However, these signals can then trigger activation of downstream protein cascades that can last from milliseconds to hours. Recent imaging studies provide many insights into the biochemical processes governing signaling events of molecular assemblies at different spatial localizations. Here, we highlight recent findings of signaling dynamics during synaptic plasticity and discuss their roles in long-term structural plasticity of dendritic spines.

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Section: Transient Ca2+ Elevation: the Trigger Of Multiple Signaling mentioning

confidence: 99%

Section: Transient Ca2+ Elevation: the Trigger Of Multiple Signaling mentioning

confidence: 99%

Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization

Nakahata

Yasuda

2018

Front. Synaptic Neurosci.

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177

161

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“…However, the duration and time window of CaMKII activity required for functional and structural plasticity remain controversial. The Yasuda group addressed this question by using an optogenetic tool to inhibit CaMKII activity spatiotemporally . They fused autocamitide inhibitory peptide 2 (AIP2), a potent CaMKII inhibitory peptide, to AsLOV2‐Jα helix, and called this fused complex paAIP2.…”

Section: Figurementioning

confidence: 99%

“…The Yasuda group addressed this question by using an optogenetic tool to inhibit CaMKII activity spatiotemporally. [65] They fused autocamitide inhibitory peptide 2( AIP2), ap otent CaMKII inhibitory peptide, to AsLOV2-Ja helix, and called this fused complex paAIP2. In the dark state, AIP2i sc aged by the Ja helix in AsLOV2 and does not function.…”

Section: Neurosciencementioning

confidence: 99%

Induction of Signal Transduction by Using Non‐Channelrhodopsin‐Type Optogenetic Tools

Ueda

Sato

2018

ChemBioChem

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Signal transductions are the basis for all cellular functions. Previous studies investigating signal transductions mainly relied on pharmacological inhibition, RNA interference, and constitutive active/dominant negative protein expression systems. However, such studies do not allow the modulation of protein activity with high spatial and temporal precision in cells, tissues, and organs in animals. Recently, non-channelrhodopsin-type optogenetic tools for regulating signal transduction have emerged. These photoswitches address several disadvantages of previous techniques, and allow us to control a variety of signal transductions such as cell membrane dynamics, calcium signaling, lipid signaling, and apoptosis. In this review we summarize recent advances in the development of such photoswitches and in how these optotools are applied to signaling processes.

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“…The increase in calcium concentration after LTP induction leads to CaMKII autophosphorylation, an event that makes CaMKII activity persist even after the decay of calcium concentration (Lisman et al, 2002 , 2012 ; Colbran and Brown, 2004 ). However, it has been demonstrated that this autonomous activity is only transient (Lengyel et al, 2004 ; Otmakhov et al, 2015 ; Murakoshi et al, 2017 ), while Thr286 phosphorylation has been proved as a persistent event, that has been observed up to 8 h after stimulation (Ahmed and Frey, 2005 ). In this regard, it has been observed that synaptic potentiation in hippocampal CA1 region is reverted when ant-CaMKIINtide, a noncompetitive inhibitor of CaMKII, is applied during the maintenance phase of CA1-LTP in vitro (Sanhueza et al, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

2017

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Calcium-calmodulin/dependent protein kinase II (CaMKII) plays an essential role in LTP induction, but since it has the capacity to remain persistently activated even after the decay of external stimuli it has been proposed that it can also be necessary for LTP maintenance and therefore for memory persistence. It has been shown that basolateral amygdaloid nucleus (Bla) stimulation induces long-term potentiation (LTP) in the insular cortex (IC), a neocortical region implicated in the acquisition and retention of conditioned taste aversion (CTA). Our previous studies have demonstrated that induction of LTP in the Bla-IC pathway before CTA training increased the retention of this task. Although it is known that IC-LTP induction and CTA consolidation share similar molecular mechanisms, little is known about the molecular actors that underlie their maintenance. The purpose of the present study was to evaluate the role of CaMKII in the maintenance of in vivo Bla-IC LTP as well as in the persistence of CTA long-term memory (LTM). Our results show that acute microinfusion of myr-CaMKIINtide, a selective inhibitor of CaMKII, in the IC of adult rats during the late-phase of in vivo Bla-IC LTP blocked its maintenance. Moreover, the intracortical inhibition of CaMKII 24 h after CTA acquisition impairs CTA-LTM persistence. Together these results indicate that CaMKII is a central key component for the maintenance of neocortical synaptic plasticity as well as for persistence of CTA-LTM.

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Kinetics of Endogenous CaMKII Required for Synaptic Plasticity Revealed by Optogenetic Kinase Inhibitor

Cited by 26 publications

References 0 publications

Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization

Plasticity of Spine Structure: Local Signaling, Translation and Cytoskeletal Reorganization

Induction of Signal Transduction by Using Non‐Channelrhodopsin‐Type Optogenetic Tools

CaMKII Requirement for in Vivo Insular Cortex LTP Maintenance and CTA Memory Persistence

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