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PLoS Biol. 2015 Jun 22;13(6):e1002181. doi: 10.1371/journal.pbio.1002181. eCollection 2015.

Ryanodine Receptor Activation Induces Long-Term Plasticity of Spine Calcium Dynamics.

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  • 1Neuroscience Research Center, Charité-Universitätsmedizin, Berlin, Germany; Berlin Institute of Health (BIH), Berlin, Germany.
  • 2Neuroscience Research Center, Charité-Universitätsmedizin, Berlin, Germany.
  • 3Institute of Physics, Humboldt Universität, Berlin, Germany.
  • 4Neuroscience Research Center, Charité-Universitätsmedizin, Berlin, Germany; Bernstein Center for Computational Neuroscience, Berlin, Germany; Cluster of Excellence 'NeuroCure', Charité-Universitätsmedizin, Berlin, Germany; DZNE- German Center for Neurodegenerative Diseases, Berlin, Germany.


A key feature of signalling in dendritic spines is the synapse-specific transduction of short electrical signals into biochemical responses. Ca2+ is a major upstream effector in this transduction cascade, serving both as a depolarising electrical charge carrier at the membrane and an intracellular second messenger. Upon action potential firing, the majority of spines are subject to global back-propagating action potential (bAP) Ca2+ transients. These transients translate neuronal suprathreshold activation into intracellular biochemical events. Using a combination of electrophysiology, two-photon Ca2+ imaging, and modelling, we demonstrate that bAPs are electrochemically coupled to Ca2+ release from intracellular stores via ryanodine receptors (RyRs). We describe a new function mediated by spine RyRs: the activity-dependent long-term enhancement of the bAP-Ca2+ transient. Spines regulate bAP Ca2+ influx independent of each other, as bAP-Ca2+ transient enhancement is compartmentalized and independent of the dendritic Ca2+ transient. Furthermore, this functional state change depends exclusively on bAPs travelling antidromically into dendrites and spines. Induction, but not expression, of bAP-Ca2+ transient enhancement is a spine-specific function of the RyR. We demonstrate that RyRs can form specific Ca2+ signalling nanodomains within single spines. Functionally, RyR mediated Ca2+ release in these nanodomains induces a new form of Ca2+ transient plasticity that constitutes a spine specific storage mechanism of neuronal suprathreshold activity patterns.

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