Dendritic, delayed, stochastic CaMKII activation in behavioural time scale plasticity

Anant Jain, Yoshihisa Nakahata, Tristano Pancani, Tetsuya Watabe, Polina Rusina, Kelly South, Kengo Adachi, Long Yan, Noriko Simorowski, Hiro Furukawa and Ryohei Yasuda ()
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Anant Jain: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Yoshihisa Nakahata: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Tristano Pancani: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Tetsuya Watabe: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Polina Rusina: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Kelly South: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Kengo Adachi: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Long Yan: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience
Noriko Simorowski: W.M. Keck Structural Biology Laboratory, Cold Spring Harbor Laboratory
Hiro Furukawa: W.M. Keck Structural Biology Laboratory, Cold Spring Harbor Laboratory
Ryohei Yasuda: Neuronal Signal Transduction Group, Max Planck Florida Institute for Neuroscience

Nature, 2024, vol. 635, issue 8037, 151-159

Abstract: Abstract Behavioural time scale plasticity (BTSP) is non-Hebbian plasticity induced by integrating presynaptic and postsynaptic components separated by a behaviourally relevant time scale (seconds)1. BTSP in hippocampal CA1 neurons underlies place cell formation. However, the molecular mechanisms that enable synapse-specific plasticity on a behavioural time scale are unknown. Here we show that BTSP can be induced in a single dendritic spine using two-photon glutamate uncaging paired with postsynaptic current injection temporally separated by a behavioural time scale. Using an improved Ca2+/calmodulin-dependent kinase II (CaMKII) sensor, we did not detect CaMKII activation during this BTSP induction. Instead, we observed dendritic, delayed and stochastic CaMKII activation (DDSC) associated with Ca2+ influx and plateau potentials 10–100 s after BTSP induction. DDSC required both presynaptic and postsynaptic activity, which suggests that CaMKII can integrate these two signals. Also, optogenetically blocking CaMKII 15–30 s after the BTSP protocol inhibited synaptic potentiation, which indicated that DDSC is an essential mechanism of BTSP. IP3-dependent intracellular Ca2+ release facilitated both DDSC and BTSP. Thus, our study suggests that non-synapse-specific CaMKII activation provides an instructive signal with an extensive time window over tens of seconds during BTSP.

Date: 2024
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DOI: 10.1038/s41586-024-08021-8

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