This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Synaptic plasticity refers to changes in strengths of the connections through which neurons communicate. Long-term synaptic plasticity, including spike-timing dependent plasticity (STDP), is believed to be the basis for learning and memory. However, the precise molecular pathways through which neuronal activity patterns are detected and translated into long-term plasticity outcomes remain to be fully elucidated. We have shown previously that a phenomenological model detector system based on biologically plausible molecular pathways can convert the time course of the calcium signal in a postsynaptic cell into synaptic strength changes consistent with experimental results from STDP and other plasticity protocols (Rubin et al., J. Neurophysiol., 2005). This project aims to incorporate spatial features of the calcium profile, together with specific molecular components, into the model, to make predictions about the roles of distinct calcium entry channels and baseline spatial distributions of key molecules in determining plasticity outcomes. We have set up code to perform biologically detailed simulations, including calcium entry and binding of calcium with downstream molecules, in the MCell environment. We would like supercomputing time to allow for incorporation of additional molecules and molecule states into the model and to make longer simulation times feasible. Following an initial meeting with Dr. Stiles, an allocation of 10,000 computational units is requested on the SALK cluster at the Pittsburgh Supercomputing Center
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