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Department of Cell and Neurobiology, Humboldt University Hospital (Charité), Institute of Anatomy, 10115 Berlin, Germany;
* Department of Neurobiology, German Primate Center, 37077 Göttingen, Germany; and
Department of Psychiatry, UT Southwestern Medical Center, Dallas, Texas 75390, USA
2Correspondence: Institute of Anatomy, Department of Cell and Neurobiology, Humboldt University Hospital (Charité), Philippstr. 12, 10098 Berlin, Germany. E-mail: robert.nitsch{at}charite.de
Differential display of hippocampal tissue after entorhinal cortex lesion (ECL) revealed decreases in mRNA encoding the neuronal hyperpolarization-activated, cyclic nucleotide-gated channel HCN1. In situ hybridization confirmed that hippocampal transcripts of HCN1, but not HCN2/3/4, are down-regulated after ECL. Expression recovered at 
21 days after lesion (dal). Immunohistochemistry demonstrated a corresponding regulation of HCN1 protein expression in CA1-CA3 dendrites, hilar mossy cells and interneurons, and granule cells. Patch-clamp recordings in the early phase after lesion from mossy cells and hilar interneurons revealed an increase in the fast time constant of current activation and a profound negative shift in voltage activation of Ih. Whereas current activation recovered at 30 dal, the voltage activation remained hyperpolarized in mossy cells and hilar interneurons. Granule cells, however, were devoid of any detectable somatic Ih currents. Hence, denervation of the hippocampus decreases HCN1 and concomitantly the Ih activity in hilar neurons, and the recovery of h-current activation kinetics occurs parallel to postlesion sprouting.—Bräuer, A. U., Savaskan, N. E., Kole, M. H. P., Plaschke, M., Monteggia, L. M., Nestler, E. J., Simbürger, E., Deisz, R. A., Ninnemann, O., Nitsch, R. Molecular and functional analysis of hyperpolarization-activated pacemaker channels in the hippocampus after entorhinal cortex lesion.
Key Words: DDRT-PCR/ECL • HCN • hippocampus • Ih
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