Dendritic excitations govern back-propagation via a spike-rate accelerometer

Pojeong Park, J. David Wong-Campos, Daniel G. Itkis, Byung Hun Lee, Yitong Qi, Hunter C. Davis, Benjamin Antin, Amol Pasarkar, Jonathan B. Grimm, Sarah E. Plutkis, Katie L. Holland, Liam Paninski, Luke D. Lavis and Adam E. Cohen ()
Additional contact information
Pojeong Park: Harvard University
J. David Wong-Campos: Harvard University
Daniel G. Itkis: Harvard University
Byung Hun Lee: Harvard University
Yitong Qi: Harvard University
Hunter C. Davis: Harvard University
Benjamin Antin: Columbia University
Amol Pasarkar: Columbia University
Jonathan B. Grimm: Howard Hughes Medical Institute
Sarah E. Plutkis: Howard Hughes Medical Institute
Katie L. Holland: Howard Hughes Medical Institute
Liam Paninski: Columbia University
Luke D. Lavis: Howard Hughes Medical Institute
Adam E. Cohen: Harvard University

Nature Communications, 2025, vol. 16, issue 1, 1-20

Abstract: Abstract Dendrites on neurons support electrical excitations, but the computational significance of these events is not well understood. We developed molecular, optical, and computational tools for all-optical electrophysiology in dendrites. We mapped sub-millisecond voltage dynamics throughout the dendritic trees of CA1 pyramidal neurons under diverse optogenetic and synaptic stimulus patterns, in acute brain slices. Our data show history-dependent spike back-propagation in distal dendrites, driven by locally generated Na+ spikes (dSpikes). Dendritic depolarization created a transient window for dSpike propagation, opened by A-type KV channel inactivation, and closed by slow NaV inactivation. Collisions of dSpikes with synaptic inputs triggered calcium channel and N-methyl-D-aspartate receptor (NMDAR)-dependent dendritic plateau potentials and accompanying complex spikes at the soma. This hierarchical ion channel network acts as a spike-rate accelerometer, providing an intuitive picture connecting dendritic biophysics to associative plasticity rules.

Date: 2025
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DOI: 10.1038/s41467-025-55819-9

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