Dynamic actin filaments are required for stable long-term potentiation (LTP) in area CA1 of the hippocampus

TLDR

The study tested whether dynamic actin filaments contribute to synaptic plasticity at the Schaffer‑collateral‑CA1 synapse in mouse hippocampus. Low concentrations (0.01–1 µM) of actin‑assembly inhibitors were bath applied to hippocampal slices while recording field EPSPs. Inhibitors cytochalasin D, B, and latrunculin A impaired LTP maintenance without affecting basal transmission, induction, or post‑tetanic potentiation, and the effect of cytochalasin B was reversible, supporting a role for dynamic actin in early LTP maintenance.

Abstract

The hypothesis that dynamic actin filaments participate in specific aspects of synaptic plasticity was investigated at the Schaffer-collateral-CA1 pyramidal cell synapse of mouse hippocampus. Low concentrations (0.01–1 μM) of compounds that inhibit actin filament assembly were bath applied to hippocampal slices during extracellular recording of field excitatory postsynaptic potentials. Cytochalasin D, cytochalasin B, and latrunculin A all impaired the maintenance of LTP induced by brief high-frequency stimulation. This effect on LTP maintenance was specific, because none of the compounds affected basal synaptic transmission, paired-pulse facilitation, LTP induction, or post-tetanic potentiation. The effect of cytochalasin B was reversible. The results are consistent with a model in which dynamic actin filaments play an essential role in the molecular mechanisms underlying the early maintenance phase of LTP, such as growth of new synaptic connections or conversion of silent synapses.