Author

Jacqueline Montanaro

Institute of Science and Technology Austria

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Neuroscience· 3

Signature Assays, Organisms & Methods

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Assay:electronic health records· 3 Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 2 Approach:statistical model· 1

Frequent Co-Authors

Ryuichi ShigemotoiD· 3 shared Stefan HallermanniD· 2 shared Abdelmoneim EshraiD· 1 shared Ákos KulikiD· 1 shared Andrea TrevisioliD· 1 shared Andreas Ritzau‐JostiD· 1 shared Bernhard BettleriD· 1 shared Christian D. WerneriD· 1 shared

Activity by Year

2019-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 21 mutual co-author links

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3 shared papersNeuroscience

Ryuichi ShigemotoORCID

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3 papers

Recent·Most cited

LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and increased action potential broadening

Andreas Ritzau‐Jost, Felix Gsell, Josefine Sell, Stefan Sachs, Jacqueline Montanaro, Toni Kirmann, Sebastian Maaß, Sarosh R. Irani, Christian D. Werner, Christian Geis, Markus Sauer, Ryuichi Shigemoto, Stefan Hallermann

This study investigates how LGI1 autoantibodies enhance synaptic transmission by reducing Kv1 channel density and broadening presynaptic action potentials.

Neurology Neuroimmunology & Neuroinflammation · Aug 14, 2024Peer-reviewedNeuroscience

GABAB receptor auxiliary subunits modulate Cav2.3-mediated release from medial habenula terminals

Pradeep Bhandari, David H. F. Vandael, Diego Fernández‐Fernández, Thorsten Fritzius, David Kleindienst, Cihan Önal, Jacqueline Montanaro, Martin Gassmann, Péter Jónás, Ákos Kulik, Bernhard Bettler, Ryuichi Shigemoto, Peter Koppensteiner

The paper investigates how GABAB receptor auxiliary subunits modulate Cav2.3-mediated neurotransmitter release in medial habenula terminals, revealing their role in synaptic strength regulation.

eLife · Apr 29, 2021Peer-reviewedNeuroscience

HCN channel-mediated neuromodulation can control action potential velocity and fidelity in central axons

Niklas Byczkowicz, Abdelmoneim Eshra, Jacqueline Montanaro, Andrea Trevisiol, Johannes Hirrlinger, Maarten H. P. Kole, Ryuichi Shigemoto, Stefan Hallermann

This study shows HCN channels modulate action potential velocity and fidelity in central axons through cAMP and neuromodulators, with implications for energy consumption and temporal delays.

eLife · Sep 6, 2019Peer-reviewedNeuroscience