Molecular and functional analysis of hyperpolarization-activated pacemaker channels in the hippocampus after entorhinal cortex lesion
Autor: | Eric J. Nestler, Martina Plaschke, Robert Nitsch, Olaf Ninnemann, Nicolai E. Savaskan, Anja U. Bräuer, Maarten H. P. Kole, Eva SimbÜRger, Lisa M. Monteggia, Rudolf A. Deisz |
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Přispěvatelé: | Other departments |
Rok vydání: | 2001 |
Předmět: |
Male
endocrine system Potassium Channels Time Factors Cyclic Nucleotide-Gated Cation Channels Hippocampal formation Biology Biochemistry Hippocampus Ion Channels Membrane Potentials Lesion Genetics medicine Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels Animals Entorhinal Cortex RNA Messenger Rats Wistar Molecular Biology In Situ Hybridization Neurons Messenger RNA Differential display Kainic Acid Reverse Transcriptase Polymerase Chain Reaction Anatomy Hyperpolarization (biology) Entorhinal cortex Rats Microscopy Electron nervous system Gene Expression Regulation Dentate Gyrus RNA medicine.symptom Neuroscience Biotechnology |
Zdroj: | FASEB journal, 15(14), 2689-2701. FASEB |
ISSN: | 1530-6860 0892-6638 |
Popis: | 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 approximately 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. |
Databáze: | OpenAIRE |
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