Mossy fiber sprouting into the hippocampal region CA2 in patients with temporal lobe epilepsy.


Journal

Hippocampus
ISSN: 1098-1063
Titre abrégé: Hippocampus
Pays: United States
ID NLM: 9108167

Informations de publication

Date de publication:
06 2021
Historique:
revised: 23 02 2021
received: 07 10 2020
accepted: 27 02 2021
pubmed: 16 3 2021
medline: 25 2 2022
entrez: 15 3 2021
Statut: ppublish

Résumé

Hippocampal sclerosis (HS) in Temporal Lobe Epilepsy (TLE) shows neuronal death in cornu ammonis (CA)1, CA3, and CA4. It is known that granule cells and CA2 neurons survive and their axons, the mossy fibers (MF), lose their target cells in CA3 and CA4 and sprout to the granule cell layer and molecular layer. We examined in TLE patients and in a mouse epilepsy model, whether MF sprouting is directed to the dentate gyrus or extends to distant CA regions and whether sprouting is associated with death of target neurons in CA3 and CA4. In 319 TLE patients, HS was evaluated by Wyler grade and International League against Epilepsy (ILAE) types using immunohistochemistry against neuronal nuclei (NeuN). Synaptoporin was used to colocalize MF. In addition, transgenic Thy1-eGFP mice were intrahippocampally injected with kainate and sprouting of eGFP-positive MFs was analyzed together with immunocytochemistry for regulator of G-protein signaling 14 (RGS14). In human HS Wyler III and IV as well as in ILAE 1, 2, and 3 specimens, we found synaptoporin-positive axon terminals in CA2 and even in CA1, associated with the extent of granule cell dispersion. Sprouting was seen in cases with cell death of target neurons in CA3 and CA4 (classical severe HS ILAE type 1) but also without this cell death (atypical HS ILAE type 2). Similarly, in epileptic mice eGFP-positive MFs sprouted to CA2 and beyond. The presence of MF terminals in the CA2 pyramidal cell layer and in CA1 was also correlated with the extent of granule cell dispersion. The similarity of our findings in human specimens and in the mouse model highlights the importance and opens up new chances of using translational approaches to determine mechanisms underlying TLE.

Identifiants

pubmed: 33720466
doi: 10.1002/hipo.23323
doi:

Substances chimiques

RGS Proteins 0
Rgs14 protein, mouse 0
Kainic Acid SIV03811UC

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

580-592

Informations de copyright

© 2021 The Authors. Hippocampus published by Wiley Periodicals LLC.

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Auteurs

Thomas M Freiman (TM)

Department of Neurosurgery, Rostock University Medical Center, Rostock, Germany.

Ute Häussler (U)

Department of Neurosurgery, Experimental Epilepsy Research, Medical Center-University of Freiburg, Faculty of Medicine, Freiburg, Germany.
Faculty of Medicine, Center for Basics in NeuroModulation, University of Freiburg, Freiburg, Germany.
BrainLinks-BrainTools Center, University of Freiburg, Freiburg, Germany.

Josef Zentner (J)

Faculty of Medicine, Department of Neurosurgery, Medical Center-University of Freiburg, Freiburg, Germany.

Soroush Doostkam (S)

Faculty of Medicine, Institute of Neuropathology, Medical Center-University of Freiburg, Freiburg, Germany.

Jürgen Beck (J)

Faculty of Medicine, Department of Neurosurgery, Medical Center-University of Freiburg, Freiburg, Germany.

Christian Scheiwe (C)

Faculty of Medicine, Department of Neurosurgery, Medical Center-University of Freiburg, Freiburg, Germany.

Armin Brandt (A)

Epilepsy Center, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.

Carola A Haas (CA)

Department of Neurosurgery, Experimental Epilepsy Research, Medical Center-University of Freiburg, Faculty of Medicine, Freiburg, Germany.
Faculty of Medicine, Center for Basics in NeuroModulation, University of Freiburg, Freiburg, Germany.
BrainLinks-BrainTools Center, University of Freiburg, Freiburg, Germany.

Barbara Puhahn-Schmeiser (B)

Faculty of Medicine, Department of Neurosurgery, Medical Center-University of Freiburg, Freiburg, Germany.

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