@article {45927,
	title = {Action potential bursting in subicular pyramidal neurons is driven by a calcium tail current.},
	journal = {J Neurosci},
	volume = {21},
	year = {2001},
	month = {2001 May 15},
	pages = {3312-21},
	abstract = {<p>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.</p>
},
	keywords = {Action Potentials, Animals, Calcium, Calcium Channel Blockers, Calcium Channels, T-Type, Dendrites, Dose-Response Relationship, Drug, Electric Stimulation, Fluorescent Dyes, Fura-2, Hippocampus, In Vitro Techniques, Microelectrodes, Microinjections, Nickel, Patch-Clamp Techniques, Perfusion, Potassium Channels, Pyramidal Cells, Rats, Sodium Channels, Tetrodotoxin},
	issn = {1529-2401},
	author = {Jung, H Y and Staff, N P and Spruston, N}
}
