Neurons have both a fast and slow mode of signaling. Fast signals are communicated by transmembrane voltage changes, while calcium levels within the cell communicate information on a much slower time scale. Calcium acts as a second messenger responsible for modulating neuronal excitability in many ways including the mediation of gene transcription in the cell and the sensitivity of the cell to further stimulus. I develop a voltage model of the neuron's electrical signal with ion diffusion and drift which includes voltage-gated calcium currents and calcium-dependent potassium currents. The influx of calcium resulting from the voltage model will prime the endoplasmic reticulum with calcium. A model of the dynamics of calcium induced calcium release from the endoplasmic reticulum via IP3 receptors which includes diffusion of calcium and IP3 as well as calcium buffering by the mitochondria results in a calcium wave similar to what has been observed experimentally.