Author

Matthew E. Larsen

University of Colorado AnschutzORCID 0000-0002-9881-7822Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2

Signature Assays, Organisms & Methods

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

Frequent Co-Authors

Karl Ulrich BayeriD· 2 shared C. Madison BarkeriD· 1 shared Hai Qian· 1 shared Johannes Wilhelm HelliD· 1 shared Olivia R. BuonaratiiD· 1 shared Raul Satoshi VargasiD· 1 shared Steven J. CoultrapiD· 1 shared

Activity by Year

2022-2026 · peak 1/yr

Co-Author Collaboration Network

7 top collaborators · 12 mutual co-author links

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2 shared papersNeuroscience

Karl Ulrich BayerORCID

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2 papers

Recent·Most cited

NeuroscienceMolecular PharmacologyPeer-reviewedMay 1, 2026

The CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding

Matthew E. Larsen, C. Madison Barker, Raul Satoshi Vargas…·Karl Ulrich Bayer

The paper shows the CaMKII D135N mutation blocks kinase activity and reduces GluN2B binding, supporting structural rather than enzymatic function in LTP.

DOI 10.1016/j.molpha.2026.100127

experimental assay

𝕏 PostBluesky

NeurosciencebioRxivPreprintJun 23, 2022

CaMKII binding to GluN2B flips a β-adrenergic switch from synaptic depression to potentiation

Olivia R. Buonarati, Matthew E. Larsen, Hai Qian…·Karl Ulrich Bayer

Buonarati et al. show that β-adrenergic stimulation enables LTP induction in response to LTD stimuli by switching synaptic CaMKII movement to LTP mode.

DOI 10.1101/2022.06.23.497296

mouseelectronic health records

𝕏 PostBluesky