Dendritic K ⁺ channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons

TLDR

The study examined whether A‑type K⁺ channels influence induction of long‑term potentiation at Schaffer collateral–CA1 synapses. LTP was induced by pairing low‑amplitude EPSPs with two postsynaptic spikes in a theta‑burst pattern, dependent on NMDA receptors. Back‑propagating action potentials were amplified in dendrites only when coincident with EPSPs, and MAPK inhibition shifted K⁺ channel activation, reduced this amplification and blocked LTP, confirming that dendritic K⁺ channels and AP boosting are essential for LTP induction.

Abstract

We investigated the role of A-type K + channels for the induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal neurons. When low-amplitude excitatory postsynaptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern, N -methyl- d -aspartate (NMDA)-receptor-dependent LTP was induced. The amplitudes of the back-propagating action potentials were boosted in the dendrites only when they were coincident with the EPSPs. Mitogen-activated protein kinase (MAPK) inhibitors PD 098059 or U0126 shifted the activation of dendritic K + channels to more hyperpolarized potentials, reduced the boosting of dendritic action potentials by EPSPs, and suppressed the induction of LTP. These results support the hypothesis that dendritic K + channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons.