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The Journal of Neuroscience, October 15, 1999, 19(20):8789-8798
Dendritic Calcium Spike Initiation and Repolarization Are
Controlled by Distinct Potassium Channel Subtypes in CA1 Pyramidal
Neurons
Nace L.
Golding,
Hae-yoon
Jung,
Timothy
Mickus, and
Nelson
Spruston
Department of Neurobiology and Physiology, Institute for
Neuroscience, Northwestern University, Evanston, Illinois 60208
In CA1 pyramidal neurons of the hippocampus, calcium-dependent
spikes occur in vivo during specific behavioral states
and may be enhanced during epileptiform activity. However, the
mechanisms that control calcium spike initiation and repolarization are
poorly understood. Using dendritic and somatic patch-pipette
recordings, we show that calcium spikes are initiated in the apical
dendrites of CA1 pyramidal neurons and drive bursts of sodium-dependent action potentials at the soma. Initiation of calcium spikes at the soma
was suppressed in part by potassium channels activated by
sodium-dependent action potentials. Low-threshold, putative D-type
potassium channels [blocked by 100 µM 4-aminopyridine
(4-AP) and 0.5-1 µM -dendrotoxin ( -DTX)]
played a prominent role in setting a high threshold for somatic calcium
spikes, thus restricting initiation to the dendrites. DTX- and
4-AP-sensitive channels were activated during sodium-dependent action
potentials and mediated a large component of their
afterhyperpolarization. Once initiated, repetitive firing of calcium
spikes was limited by activation of putative BK-type calcium-activated
potassium channels (blocked by 250 µM tetraethylammonium
chloride, 70 nM charybdotoxin, or 100 nM
iberiotoxin). Thus, the concerted action of calcium- and voltage-activated potassium channels serves to focus spatially and
temporally the membrane depolarization and calcium influx generated by
calcium spikes during strong, synchronous network excitation.
Key words:
bursting; calcium spike; BK channels; dendrotoxin; 4-AP; TEA; hippocampus
Copyright © 1999 Society for Neuroscience 0270-6474/99/19208789-10$05.00/0
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