Description:

The department of Physiology welcomes Ulli Bayer, Ph.D.

The Calcium/calmodulin-dependent protein kinase II (CaMKII) can be made “autonomous” (calcium-independent) by autophosphorylation at T286, a mechanism that has been regarded as molecular memory. Indeed, CaMKII its autonomous activity is prominently involved in mediating long-term potentiation of synaptic strength (LTP), a form of synaptic plasticity thought to be required for learning and memory. Our more recent work has shown that CaMKII and T286 phosphorylation also mediates the opposite form of synaptic plasticity (LTD) as well as excitotoxic neuronal cell death (induced by glutamate in vitro or by cardiac arrest and CPR in vivo). This seminar will discuss these recap these past findings, and provide mechanistic information how the decision between these different signaling outcomes is directed by the competitive interaction of CaMKII and DAPK1 with the GluN2B subunit of the NMDA receptor.