Dendritic Branch-constrained N-Methyl-D-Aspartate Receptor-mediated Spikes Drive Synaptic Plasticity in Hippocampal CA3 Pyramidal Cells

N-methyl-D-aspartate receptor-mediated ( spikes can be causally linked to the induction of synaptic long-term potentiation (LTP) in hippocampal and cortical pyramidal cells. However, it is unclear if they regulate plasticity at a local or global scale in the dendritic tree. Here, we used dendritic patch-clamp recordings and calcium imaging to investigate the integrative properties of single dendrites of hippocampal CA3 cells. We show that local hyperpolarization of a single dendritic segment prevents NMDA spikes, their associated calcium transients, as well as LTP in a branch-specific manner. This result provides direct, causal evidence that the single dendritic branch can operate as a functional unit in regulating CA3 pyramidal cell plasticity. This article is part of a Special Issue entitled: SI: Dendritic contributions to biological and artificial computations. (C) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

Automated summary

In this study, dendritic patch-clamp recordings and calcium imaging were used to investigate the integrative properties of single dendrites. It was found that local hyperpolarization of a single dendritic segment can prevent NMDA spikes, their associated calcium transients, and LTP in a branch-specific manner. This finding provides direct evidence that a single dendritic branch operates as a functional unit in regulating CA3 pyramidal cell plasticity.