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This Article Full Text Full Text (PDF) All Versions of this Article: 97/5/3242    most recent 00422.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Fernández de Sevilla, D. Articles by Buño, W. Search for Related Content PubMed PubMed Citation Articles by Fernández de Sevilla, D. Articles by Buño, W.

Selective Shunting of the NMDA EPSP Component by the Slow Afterhyperpolarization in Rat CA1 Pyramidal Neurons

¹Instituto Cajal, Consejo Superior de Investigaciones Cientificas, Madrid; and ²Departamento de Tecnologías de la Información y las Comunicaciones, Universidad de la Coruña, La Coruña, Spain

Submitted 21 April 2006; accepted in final form 13 February 2007

Pyramidal neuron dendrites express voltage-gated conductances that control synaptic integration and plasticity, but the contribution of the Ca²⁺-activated K⁺-mediated currents to dendritic function is not well understood. Using dendritic and somatic recordings in rat hippocampal CA1 pyramidal neurons in vitro, we analyzed the changes induced by the slow Ca²⁺-activated K⁺-mediated afterhyperpolarization (sAHP) generated by bursts of action potentials on excitatory postsynaptic potentials (EPSPs) evoked at the apical dendrites by perforant path-Schaffer collateral stimulation. Both the amplitude and decay time constants of EPSPs (_EPSP) were reduced by the sAHP in somatic recordings. In contrast, the dendritic EPSP amplitude remained unchanged, whereas _EPSP was reduced. Temporal summation was reduced and spatial summation linearized by the sAHP. The amplitude of the isolated N-methyl-D-aspartate component of EPSPs (EPSP_NMDA) was reduced, whereas _NMDA was unaffected by the sAHP. In contrast, the sAHP did not modify the amplitude of the isolated EPSP_AMPA but reduced _AMPA both in dendritic and somatic recordings. These changes are attributable to a conductance increase that acted mainly via a selective "shunt" of EPSP_NMDA because they were absent under voltage clamp, not present with imposed hyperpolarization simulating the sAHP, missing when the sAHP was inhibited with isoproterenol, and reduced under block of EPSP_NMDA. EPSPs generated at the basal dendrites were similarly modified by the sAHP, suggesting both a somatic and apical dendritic location of the sAHP channels. Therefore the sAHP may play a decisive role in the dendrites by regulating synaptic efficacy and temporal and spatial summation.

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