Our field is molecular and cellular neuroscience. Specifically, we are interested in the molecular and cellular mechanisms underlying learning, memory and cognition. These higher brain functions are thought to require “synaptic plasticity”, i.e. changes in the strength of the synapses that form the connections between neurons. We are studying the mechanisms by which such changes at individual synapses are initiated and maintained. The main forms of plasticity that we are studying are long-term potentiation (LTP) and long-term depression (LTD) of excitatory synapses in the hippocampus, a brain region required for declarative learning and memory. We are also interested in how changes at one synapse are communicated to other nearby synapses. For instance, how do excitatory LTD-stimuli also cause long-term potentiation of inhibitory synapses (iLTP) on the dendrites of the same neuron?
Selected Research Articles(of >60): (*: as corresponding author, even if not listed last)
* Cook, S. G., Buonarati, O. R., Coultrap, S. J., and Bayer, K. U. (2021) CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision. Science Advances. 7: eabe2300 https://advances.sciencemag.org/content/7/16/eabe2300
* Buonarati, O. R., Cook, S. G., Goodell, D. J., Chalmers, N. E., Rumian, N. L. Tullis., J. E., Restrepo, S, Coultrap, S. J., Quillinan, N., Herson, P. S., and Bayer, K. U. (2020) CaMKII versus DAPK1 binding to GluN2B in ischemic neuronal cell death after resuscitation from cardiac arrest. Cell Reports. 30: 1-8.
* Cook, S. G., Goodell, D. J., Restrepo, S., Arnold, D. B., and Bayer, K. U. (2019) Simultaneous live-imaging of three endogenous proteins reveals that β amyloid blocks the LTP-induced synaptic accumulation of CaMKII. Cell Reports. 27: 658-665. (cover article) https://doi.org/10.1016/j.celrep.2019.03.041
* Woolfrey, K., O’Leary, H., Goodell, D. J., Robertson, H., Horne, E., Coultrap, S. J., Dell’Acqua, M. L., and Bayer, K. U. (2018) CaMKII regulates the de-palmitoylation and synaptic removal of AKAP79/150 to mediate structural LTD. J. Biol. Chem. 293:1551-1567. (editor’s pick and cover article)
* Goodell, D. J., Zaegel, V., Coultrap, S. J., and Bayer, K. U. (2017) DAPK1 mediates LTD by making the CaMKII/GluN2B binding LTP-specific. Cell Reports 19:2231-2243.
* Myers, J., Zaegel, V., Coultrap, S. J., Miller, A., Bayer, K. U., and Reichow, S. L. (2017) The CaMKII holoenzyme structure in activation-competent conformations. Nature Commun. 8:15742. https://www.nature.com/articles/ncomms15742
* Deng, G., Orfila, J. E., Dietz, R. M., Moreno-Garcia, M., Coultrap, S. J., Quilinan, N., Traystman, R. J., Bayer, K. U., and Herson, P. S. (2017) Autonomous CaMKII activity as a drug target for histological and functional neuroprotection after resuscitation from cardiac arrest. Cell Reports 18:1109-1117.
* Barcomb, K., Hell, J. W. Benke, T. A., and Bayer, K. U. (2016) The CaMKII/GluN2B protein interaction maintains synaptic strength. J. Biol. Chem. 291:16082-16089.
* Coultrap, S. J., Freund, R., O’Leary, H., Sanderson, J., Roche, K., Dell’Acqua, M.L., and Bayer, K. U. (2014) Autonomous CaMKII mediates both LTP and LTD using a mechanism for differential substrate site selection. Cell Reports 6:431-437.
* Coultrap, S. J., and Bayer, K. U. (2014) Nitric oxide induces Ca2+-independent activity of the Ca2+/calmodulin-dependent protein kinase II (CaMKII). J. Biol. Chem. 289:19458-19465.
* Barcomb, K., Buard, I., Coultrap, S. J., Kulbe, J. R., O’Leary, H., Benke, T.A., and Bayer, K. U. (2014) Autonomous CaMKII requires further stimulation by Ca2+/calmodulin for enhancing synaptic strength. FASEB J. 28:3810-3819.
* Buard, I., Freund, R., Lee, Y.-S., Coultrap, S. J., Dell’Acqua, M. L., Silva, A. J., and Bayer, K. U. (2010) CaMKII "autonomy" is required for initiating but not for maintaining neuronal long-term information storage. J. Neurosci. 30:8214-8220.
* Vest, R. S., O’Leary, H., Coultrap, S. J., Kindy, M. and Bayer, K. U. (2010) Effective post-insult neuroprotection by a novel CaMKII inhibitor. J. Biol. Chem. 285:20675-20682.
* Bayer, K. U., LeBel, E., McDonald, G.L., O’Leary, H., Schulman, H. and DeKoninck, P. (2006) Transition from reversible to persistent binding of CaMKII to postsynaptic sites and NR2B. J. Neurosci.. 26:1164-1174.
* Bayer, K. U., De Koninck, P. and Schulman, H. (2002) Alternative splicing modulates the frequency-dependent response of CaMKII to Ca2+-oscillations. EMBO J., 21:3590-3597.
* Bayer, K.-U., De Koninck, P., Leonard, A.S., Hell, J.W. and Schulman, H. (2001) Interaction with the NMDA receptor locks CaMKII in an active conformation. Nature, 411:801-805.
Bayer, K.-U., Harbers, K. and Schulman, H. (1998) aKAP is an anchoring protein for a novel CaM kinase II isoform in skeletal muscle. EMBO J., 17:5598-5605.