Asymmetric Voltage Attenuation in Dendrites Can Enable Hierarchical Heterosynaptic Plasticity

Toviah Moldwin*, Menachem Kalmenson, Idan Segev

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Long-term synaptic plasticity is mediated via cytosolic calcium concentrations ([Ca2+]). Using a synaptic model that implements calcium-based long-term plasticity via two sources of Ca2+ — NMDA receptors and voltage-gated calcium channels (VGCCs) — we show in dendritic cable simulations that the interplay between these two calcium sources can result in a diverse array of heterosynaptic effects. When spatially clustered synaptic input produces a local NMDA spike, the resulting dendritic depolarization can activate VGCCs at non-activated spines, resulting in heterosynaptic plasticity. NMDA spike activation at a given dendritic location will tend to depolarize dendritic regions that are located distally to the input site more than dendritic sites that are proximal to it. This asymmetry can produce a hierarchical effect in branching dendrites, where an NMDA spike at a proximal branch can induce heterosynaptic plasticity primarily at branches that are distal to it. We also explored how simultaneously activated synaptic clusters located at different dendritic locations synergistically affect the plasticity at the active synapses, as well as the heterosynaptic plasticity of an inactive synapse “sandwiched” between them. We conclude that the inherent electrical asymmetry of dendritic trees enables sophisticated schemes for spatially targeted supervision of heterosynaptic plasticity.

Original languageEnglish
Article numberENEURO.0014-23.2023
JournaleNeuro
Volume10
Issue number7
DOIs
StatePublished - Jul 2023

Bibliographical note

Publisher Copyright:
© 2023 Moldwin et al.

Keywords

  • calcium
  • dendrites
  • heterosynaptic plasticity
  • NMDA
  • synaptic plasticity
  • VGCC

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