title: Action potential bursting in subicular pyramidal neurons is driven by a calcium tail current.
abstract: 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 Ca(2+) tail current drives bursting in subicular pyramidal neurons. An action potential activates voltage-activated Ca(2+) channels, which deactivate slowly enough during action potential repolarization to produce an afterdepolarization that triggers subsequent action potentials in the burst. The Ca(2+) channels underlying bursting are located primarily near the soma, and the amplitude of Ca(2+) tail currents correlates with the strength of bursting across cells. Multiple channel subtypes contribute to Ca(2+) tail current, but the need for an action potential to produce the slow depolarization suggests a central role for high-voltage-activated Ca(2+) channels in subicular neuron bursting.
authors.affiliation: Department of Neurobiology and Physiology, Institute for Neuroscience, Northwestern University, Evanston, Illinois 60208, USA.
authors.forename: H Y
authors.initials: HY
authors.lastname: Jung
authors.forename: N P
authors.initials: NP
authors.lastname: Staff
authors.forename: N
authors.initials: N
authors.lastname: Spruston
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type / Q000378:metabolism; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D005456:Fluorescent Dyes; D016257:Fura-2; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D066298:In Vitro Techniques; D008839:Microelectrodes; D008845:Microinjections; D009532:Nickel / Q000008:administration & dosage; D018408:Patch-Clamp Techniques; D010477:Perfusion; D015221:Potassium Channels / Q000378:metabolism; D017966:Pyramidal Cells / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D015222:Sodium Channels / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D005456:Fluorescent Dyes; D015221:Potassium Channels; D015222:Sodium Channels; D013779:Tetrodotoxin; D009532:Nickel; D002118:Calcium; D016257:Fura-2