Action potential bursting in subicular pyramidal neurons is driven by a calcium tail current

Subiculum is the primary output area of the hippocampus and serves as a key relay center in the process of memory formation and retrieval. A majority of subicular pyramidal neurons communicate via bursts of action potentials, a mode of signaling that may enhance the fidelity of information transfer and synaptic plasticity or contribute to epilepsy when unchecked. In the present study, we show that a Ca²⁺ tail current drives bursting in subicular pyramidal neurons. An action potential activates voltage-activated Ca²⁺ channels, which deactivate slowly enough during action potential repolarization to produce an afterdepolarization that triggers subsequent action potentials in the burst. The Ca²⁺ channels underlying bursting are located primarily near the soma, and the amplitude of Ca²⁺ tail currents correlates with the strength of bursting across cells. Multiple channel subtypes contribute to Ca²⁺ tail current, but the need for an action potential to produce the slow depolarization suggests a central role for high-voltage-activated Ca²⁺ channels in subicular neuron bursting.