LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening
Ritzau-Jost A, Gsell F, Sell J, Sachs S, Montanaro-Punzengruber J-C, Kirmann T, Maaß S, Irani SR, Werner C, Geis C, Sauer M, Shigemoto R, Hallermann S. 2024. LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening. Neurology, Neuroimmunology and Neuroinflammation. 11(5), e200284.
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https://doi.org/10.1212/NXI.0000000000200284
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Journal Article
| Epub ahead of print
| English
Scopus indexed
Author
Ritzau-Jost, Andreas;
Gsell, Felix;
Sell, Josefine;
Sachs, Stefan;
Montanaro-Punzengruber, Jacqueline-ClaireISTA;
Kirmann, Toni;
Maaß, Sebastian;
Irani, Sarosh R.;
Werner, Christian;
Geis, Christian;
Sauer, Markus;
Shigemoto, RyuichiISTA
All
All
Department
Abstract
Autoantibodies against the protein leucine-rich glioma inactivated 1 (LGI1) cause the most
common subtype of autoimmune encephalitis with predominant involvement of the limbic
system, associated with seizures and memory deficits. LGI1 and its receptor ADAM22 are part
of a transsynaptic protein complex that includes several proteins involved in presynaptic
neurotransmitter release and postsynaptic glutamate sensing. Autoantibodies against LGI1
increase excitatory synaptic strength, but studies that genetically disrupt the LGI1-ADAM22
complex report a reduction in postsynaptic glutamate receptor-mediated responses. Thus, the
mechanisms underlying the increased synaptic strength induced by LGI1 autoantibodies remain elusive, and the contributions of presynaptic molecules to the LGI1-transsynaptic complex remain unclear. We therefore investigated the presynaptic mechanisms that mediate
autoantibody-induced synaptic strengthening.
Publishing Year
Date Published
2024-08-14
Journal Title
Neurology, Neuroimmunology and Neuroinflammation
Acknowledgement
The authors thank Claudia Sommer for expert technical
assistance, the Electron Microscopy Facility of IST-Austria for
resources, and Tereza Belinova in the Imaging and Optics
Facility of IST-Austria for 3D reconstruction.
Acknowledged SSUs
Volume
11
Issue
5
Page
e200284
eISSN
IST-REx-ID
Cite this
Ritzau-Jost A, Gsell F, Sell J, et al. LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening. Neurology, Neuroimmunology and Neuroinflammation. 2024;11(5):e200284. doi:10.1212/NXI.0000000000200284
Ritzau-Jost, A., Gsell, F., Sell, J., Sachs, S., Montanaro-Punzengruber, J.-C., Kirmann, T., … Hallermann, S. (2024). LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening. Neurology, Neuroimmunology and Neuroinflammation. Wolters Kluwer. https://doi.org/10.1212/NXI.0000000000200284
Ritzau-Jost, Andreas, Felix Gsell, Josefine Sell, Stefan Sachs, Jacqueline-Claire Montanaro-Punzengruber, Toni Kirmann, Sebastian Maaß, et al. “LGI1 Autoantibodies Enhance Synaptic Transmission by Presynaptic Kv1 Loss and Increased Action Potential Broadening.” Neurology, Neuroimmunology and Neuroinflammation. Wolters Kluwer, 2024. https://doi.org/10.1212/NXI.0000000000200284.
A. Ritzau-Jost et al., “LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening,” Neurology, Neuroimmunology and Neuroinflammation, vol. 11, no. 5. Wolters Kluwer, p. e200284, 2024.
Ritzau-Jost A, Gsell F, Sell J, Sachs S, Montanaro-Punzengruber J-C, Kirmann T, Maaß S, Irani SR, Werner C, Geis C, Sauer M, Shigemoto R, Hallermann S. 2024. LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening. Neurology, Neuroimmunology and Neuroinflammation. 11(5), e200284.
Ritzau-Jost, Andreas, et al. “LGI1 Autoantibodies Enhance Synaptic Transmission by Presynaptic Kv1 Loss and Increased Action Potential Broadening.” Neurology, Neuroimmunology and Neuroinflammation, vol. 11, no. 5, Wolters Kluwer, 2024, p. e200284, doi:10.1212/NXI.0000000000200284.
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