Dendritic excitations govern back-propagation via a spike-rate accelerometer.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 39905023.
- Also identified by DOI 10.1038/s41467-025-55819-9 and PMC identifier 11794848.
- Licence recorded as CC BY-NC-ND.
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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<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.
Medical subject headings
- Dendrites
- Pyramidal Cells
- Action Potentials