NMDAR and CaMKII interactions in the postsynaptic neuron play crucial roles that underlie our ability to learn and form memories. Their activity varies with time and space, and elucidating this matter is important for understanding how memory works. We develop a computer model that creates realistic 3D movements and reactions of molecules within a cell. It is an isolated model that enables us to look specifically at our molecules of interest, NMDARs and CaMKII. The report aims to answer three main questions which should address: the validity of our model against previous knowledge, the effects of sub-cellular localization on CaMKII and the effects on CaMKII by abolishing CaMKII/NMDAR binding. For the first question, we compared results with published literature. Secondly, counting boxes were added to the cell to assess if PSD regions were associated with higher molecule levels compared to cytosolic regions. Lastly, a mutant model was created to account for effects of CaMKII/NMDAR binding impairments. These experiments found that our model is consistent with what is known about sequence of molecule reactions and timeline of CaMKII activation. We could not conclude that space affects CaMKII activity as suggested, but we found that abolishing the interaction between NMDARs and CaMKII increased levels of free, phosphorylated CaMKII.
Roman Garcia, Susana; Stefan, Melanie. (2017). Computational modelling and simulation of the interaction between NMDA receptors and CaMKII in the postsynaptic neuron, [dataset]. University of Edinburgh, MCell.org, Blender.org, The National Center for Multiscale Modeling of Biological Systems (MMBioS). http://dx.doi.org/10.7488/ds/2058.
|Date made available
|7 Jun 2017