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Probing plasticity

Two new studies provide new tools for examining mechanisms of plasticity in dendrites. Tang and Yasuda developed new fluorescence resonance energy transfer (FRET)-based sensors for extracellular signal-regulated kinase (ERK) and protein kinase A (PKA), which are implicated in synaptic plasticity, primarily by replacing the fluorophore pairs in existing FRET sensors. The new sensors were 2–3-fold more sensitive and allowed ERK and PKA activity to be visualized in individual dendritic spines of hippocampal neurons during structural plasticity under two-photon fluorescence lifetime imaging microscopy. Murakoshi et al. developed a genetically encoded, photo-inducible calcium/calmodulin-dependent protein kinase type II (CaMKII) inhibitor. The induction of long-term potentiation (LTP) and structural plasticity in spines requires CaMKII, but it has been hard to assess the temporal requirement of its activation in these processes. In hippocampal slices, photoactivation of the inhibitor revealed that CaMKII activation is needed early in the process of LTP induction for LTP and structural plasticity to occur. Moreover, in mice in an inhibitory avoidance task, photoactivation of the inhibitor showed that CaMKII activity was necessary in amygdalar neurons during training, but not after training completion, for the formation of memories.


  1. Tang, S. & Yasuda, R. Imaging ERK and PKA activation in single dendritic spines during structural plasticity. Neuron 93, 1315–1324 (2017)

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  2. Murakoshi, H. et al. Kinetics of endogenous CaMKII required for synaptic plasticity revealed by optogenetic kinase inhibitor. Neuron (2017)

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Yates, D. Probing plasticity. Nat Rev Neurosci 18, 266 (2017).

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