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This Article Full Text Full Text (PDF) All Versions of this Article: 580/3/787    most recent jphysiol.2006.121343v2 jphysiol.2006.121343v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Gasparini, S. Articles by Magee, J. C. Search for Related Content PubMed PubMed Citation Articles by Gasparini, S. Articles by Magee, J. C. Related Collections Neuroscience

¹ Neuroscience Center, Louisiana State University Health Science Center, New Orleans, LA 70112, USA
² Marine Biological Laboratory, Woods Hole, MA 02543, USA
³ Center for Learning and Memory, University of Texas at Austin, Austin, TX 78712, USA

Back-propagating action potentials (bAPs) are involved in associative synaptic plasticity and the modulation of dendritic excitability. We have used high-speed confocal and two-photon imaging to measure calcium and voltage signals associated with action potential propagation into oblique branches of CA1 pyramidal neurons in adult hippocampal slices. The spatial profile of the bAP-associated Ca²⁺ influx was biphasic, with an initial increase in the proximity of the branch point followed by a progressive decrease. Voltage imaging in the branches showed that bAP amplitude was initially constant and then steadily declined with distance from the soma. To determine the role of transient K⁺ channels in this profile, we used external Ba²⁺ (150 µM) as a channel blocker, after characterizing its effect on A-type K⁺ channels in the apical trunk. Bath application of Ba²⁺ significantly reduced the A-type K⁺ current in outside-out patches and nearly eliminated the distance-dependent decrease in bAP amplitude and its associated Ca²⁺ signal. Finally, small amplitude bAPs at more distal oblique branch locations could be boosted by simultaneous branch depolarization, such that the paired Ca²⁺ signal became nearly the same for proximal and distal oblique dendrites. These data suggest that dendritic K⁺ channels regulate the amplitude of bAPs to create a dendritic Ca²⁺ signal whose magnitude is inversely related to the electrotonic distance from the soma when bAPs are not associated with a significant amount of localized synaptic input. This distance-dependent Ca²⁺ signal from bAPs, however, can be amplified and a strong associative signal is produced once the proper correlation between synaptic activation and AP output is achieved. We hypothesize that these two signals may be involved in the regulation of the expression and activity of dendritic voltage- and ligand-gated ion channels.

(Received 19 September 2006; accepted after revision 31 January 2007; first published online 1 February 2007)
Corresponding author S. Gasparini: Neuroscience Center, Louisiana State University Health Science Center, 2020 Gravier Street, New Orleans, LA 70112, USA. Email: sgaspa1{at}lsuhsc.edu

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