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During the latent period of epileptogenesis, most CA1 pyramidal cells that normally fire in a regular pattern, acquire low\u2010threshold bursting behaviour, generating high\u2010frequency clusters of 3\u20135 spikes as their minimal response to depolarizing stimuli. Recruitment of a Ni<jats:sup>2+<\/jats:sup>\u2010 and amiloride\u2010sensitive T\u2010type Ca<jats:sup>2+<\/jats:sup> current (<jats:italic>I<\/jats:italic><jats:sub>CaT<\/jats:sub>), shown to be up\u2010regulated after <jats:sc>SE<\/jats:sc>, plays a critical role in burst generation in most cases. Several lines of evidence suggest that <jats:italic>I<\/jats:italic><jats:sub>CaT<\/jats:sub> driving bursting is located in the apical dendrites. Thus, bursting was suppressed by focally applying Ni<jats:sup>2+<\/jats:sup> to the apical dendrites, but not to the soma. It was also suppressed by applying either tetrodotoxin or the K<jats:sub>V<\/jats:sub>7\/M\u2010type K<jats:sup>+<\/jats:sup> channel agonist retigabine to the apical dendrites. Severing the distal apical dendrites \u223c150 \u03bc<jats:sc>m<\/jats:sc> from the pyramidal layer also abolished this activity. Intradendritic recordings indicated that evoked bursts are associated with local Ni<jats:sup>2+<\/jats:sup>\u2010sensitive slow spikes. Blocking persistent Na<jats:sup>+<\/jats:sup> current did not modify bursting in most cases. We conclude that <jats:sc>SE<\/jats:sc>\u2010induced increase in <jats:italic>I<\/jats:italic><jats:sub>CaT<\/jats:sub> density in the apical dendrites facilitates their depolarization by the backpropagating somatic spike. The <jats:italic>I<\/jats:italic><jats:sub>CaT<\/jats:sub>\u2010driven 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 <jats:italic>I<\/jats:italic><jats:sub>CaT<\/jats:sub>\u2010driven low\u2010threshold bursting in CA1 pyramidal cells that experienced <jats:sc>SE<\/jats:sc> most probably contribute to the emergence of abnormal network discharges and may also play a role in the circuitry reorganization associated with epileptogenesis.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.127670","type":"journal-article","created":{"date-parts":[[2007,2,3]],"date-time":"2007-02-03T06:41:17Z","timestamp":1170484877000},"page":"435-450","source":"Crossref","is-referenced-by-count":85,"title":["Recruitment of apical dendritic T\u2010type Ca<sup>2<\/sup><sup>+<\/sup> channels by backpropagating spikes underlies <i>de novo<\/i> intrinsic bursting in hippocampal 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