| Advances in experimental techniques have led to a recent explosion in knowledge of the properties and function of neuronal dendrites. Much new research has focused on dendritic action potentials, which are thought to play an important role in many cellular functions, including synaptic plasticity. In particular, dendritic action potentials are thought to play an important role in the recently discovered form of long-term synaptic plasticity called spike timing-dependent plasticity (STDP). Action potentials that propagate back into the dendrites are thought to influence plasticity machinery located at synapses. In this dissertation, I use computational and theoretical techniques to better understand propagation of dendritic action potentials and to uncover the underlying mechanisms responsible for the STDP phenomenon.; Propagation of dendritic action potentials is controlled by properties of dendrites, including the voltage-gated ion channel properties and dendritic morphology. Using models of CA1 pyramidal cells, we find that underlying traveling wave attractors exist and control action potential propagation in the dendrites. By computing these attractors, we study the role of the distribution and dynamics of potassium channels in controlling dendritic action potential propagation. Even in simplified dendrite models that lack branches, propagation failures are observed similar to those observed experimentally. In more realistic models, effects of branching on action potential propagation amplitude are clearly visible. However, branching in these models plays a minor role in controlling propagation compared with that of potassium channels.; Models of synaptic plasticity have been proposed to explain the recently discovered spike timing-dependent plasticity (STDP) phenomenon. However, these models, which rely completely on postsynaptic calcium levels, cannot quantitatively account for STDP. Also, predictions from these models are utterly incompatible with new data collected with increased postsynaptic calcium influx. For this reason, we propose a new mechanistic model of synaptic plasticity, based on recent experimental data. The new model is far more successful than existing models in accounting for experimental data. It captures all the known features of STDP under both control conditions and conditions of enhanced calcium influx. |
