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<p>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<sup>+</sup> spikes (dSpikes). Dendritic depolarization created a transient window for dSpike propagation, opened by A-type K<sub>V</sub> channel inactivation, and closed by slow Na<sub>V</sub> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月4日

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  • 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,
  • Adam E. Cohen

摘要

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.