Neuron
Volume 44, Issue 3, 28 October 2004, Pages 495-508
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Article
Seizure-Induced Plasticity of h Channels in Entorhinal Cortical Layer III Pyramidal Neurons

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Abstract

The entorhinal cortex (EC) provides the predominant excitatory drive to the hippocampal CA1 and subicular neurons in chronic epilepsy. Discerning the mechanisms underlying signal integration within EC neurons is essential for understanding network excitability alterations involving the hippocampus during epilepsy. Twenty-four hours following a single seizure episode when there were no behavioral or electrographic seizures, we found enhanced spontaneous activity still present in the rat EC in vivo and in vitro. The increased excitability was accompanied by a profound reduction in Ih in EC layer III neurons and a significant decline in HCN1 and HCN2 subunits that encode for h channels. Consequently, dendritic excitability was enhanced, resulting in increased neuronal firing despite hyperpolarized membrane potentials. The loss of Ih and the increased neuronal excitability persisted for 1 week following seizures. Our results suggest that dendritic Ih plays an important role in determining the excitability of EC layer III neurons and their associated neural networks.

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Present address: Department of Pharmacology, University College London, Gower Street, London, WC1E 6BT.

4

Present address: Center for Learning and Memory, Section of Neurobiology, University of Texas at Austin, 1 University Station, A1955, Austin, Texas 78712-0132.