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

• Branch-constrained dendritic NMDA spikes can be suppressed by local hyperpolarization. • Branch-constrained hyperpolarization does not suppress NMDA spikes on other dendritic branches. • The local generation of NMDA spikes can induce LTP in a branch-selective manner. 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. [ABSTRACT FROM AUTHOR]