Loss of Long-Term Potentiation at Hippocampal Output Synapses in Experimental Temporal Lobe Epilepsy.

Autor:	Grosser S; Institute of Integrative Neuroanatomy, Charité-Universitätsmedizin Berlin, Berlin, Germany., Buck N; Department of Anesthesiology and Intensive Care Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany., Braunewell KH; Department of Neurophysiology, Medical Faculty, Ruhr University Bochum, Bochum, Germany., Gilling KE; Department of Psychiatry and Psychotherapy, Charité-Universitätsmedizin Berlin, Berlin, Germany., Wozny C; Strathclyde Institute of Pharmacy and Biomedical Sciences, Faculty of Science, University of Strathclyde, Glasgow, United Kingdom., Fidzinski P; Department of Neurology with Experimental Neurology, Charité-Universitätsmedizin Berlin, Berlin, Germany., Behr J; Department of Psychiatry and Psychotherapy, Brandenburg Medical School, Neuruppin, Germany.; Department of Psychiatry and Psychotherapy, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Jazyk:	angličtina
Zdroj:	Frontiers in molecular neuroscience [Front Mol Neurosci] 2020 Aug 28; Vol. 13, pp. 143. Date of Electronic Publication: 2020 Aug 28 (Print Publication: 2020).
DOI:	10.3389/fnmol.2020.00143
Abstrakt:	Patients suffering from temporal lobe epilepsy (TLE) show severe problems in hippocampus dependent memory consolidation. Memory consolidation strongly depends on an intact dialog between the hippocampus and neocortical structures. Deficits in hippocampal signal transmission are known to provoke disturbances in memory formation. In the present study, we investigate changes of synaptic plasticity at hippocampal output structures in an experimental animal model of TLE. In pilocarpine-treated rats, we found suppressed long-term potentiation (LTP) in hippocampal and parahippocampal regions such as the subiculum and the entorhinal cortex (EC). Subsequently we focused on the subiculum, serving as the major relay station between the hippocampus proper and downstream structures. In control animals, subicular pyramidal cells express different forms of LTP depending on their intrinsic firing pattern. In line with our extracellular recordings, we could show that LTP could only be induced in a minority of subicular pyramidal neurons. We demonstrate that a well-characterized cAMP-dependent signaling pathway involved in presynaptic forms of LTP is perturbed in pilocarpine-treated animals. Our findings suggest that in TLE, disturbances of synaptic plasticity may influence the information flow between the hippocampus and the neocortex. (Copyright © 2020 Grosser, Buck, Braunewell, Gilling, Wozny, Fidzinski and Behr.)
Databáze:	MEDLINE
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