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This Article Full Text Full Text (PDF) All Versions of this Article: 580/2/435    most recent jphysiol.2007.127670v1 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 Yaari, Y. Articles by Su, H. Search for Related Content PubMed PubMed Citation Articles by Yaari, Y. Articles by Su, H. Related Collections Neuroscience

¹ Department of Physiology, Institute of Medical Sciences, Hebrew University-Hadassah School of Medicine, Jerusalem 91120, Israel

A single episode of status epilepticus (SE) induced in rodents by the convulsant pilocarpine, produces, after a latent period of 2 weeks, a chronic epileptic condition. During the latent period of epileptogenesis, most CA1 pyramidal cells that normally fire in a regular pattern, acquire low-threshold bursting behaviour, generating high-frequency clusters of 3–5 spikes as their minimal response to depolarizing stimuli. Recruitment of a Ni²⁺- and amiloride-sensitive T-type Ca²⁺ current (I_CaT), shown to be up-regulated after SE, plays a critical role in burst generation in most cases. Several lines of evidence suggest that I_CaT driving bursting is located in the apical dendrites. Thus, bursting was suppressed by focally applying Ni²⁺ to the apical dendrites, but not to the soma. It was also suppressed by applying either tetrodotoxin or the K_V7/M-type K⁺ channel agonist retigabine to the apical dendrites. Severing the distal apical dendrites 150 µM from the pyramidal layer also abolished this activity. Intradendritic recordings indicated that evoked bursts are associated with local Ni²⁺-sensitive slow spikes. Blocking persistent Na⁺ current did not modify bursting in most cases. We conclude that SE-induced increase in I_CaT density in the apical dendrites facilitates their depolarization by the backpropagating somatic spike. The I_CaT-driven dendritic depolarization, in turn, spreads towards the soma, initiating another backpropagating spike, and so forth, thereby creating a spike burst. The early appearance and predominance of I_CaT-driven low-threshold bursting in CA1 pyramidal cells that experienced SE most probably contribute to the emergence of abnormal network discharges and may also play a role in the circuitry reorganization associated with epileptogenesis.

(Received 3 January 2007; accepted after revision 24 January 2007; first published online 1 February 2007)
Corresponding author Y. Yaari: Department of Physiology, Institute of Medical Sciences, Hebrew University-Hadassah School of Medicine, PO Box 12272, Jerusalem 91121, Israel.  Email: yaari{at}md.huji.ac.il

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