The modification of neural circuits depends on the strengthening and weakening of synaptic connections. Synaptic strength is often correlated to the density of the ionotropic, glutamateric receptors, AMPAR, (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor) at the postsynaptic density (PSD). While AMPAR density is known to change based on complex biological signaling cascades, the effect of geometric factors such as dendritic spine shape, size, and curvature remain poorly understood. In this work, we developed a deterministic, spatiotemporal model to study the dynamics of AMPAR during long term potentiation (LTP). This model includes a minimal set of biochemical events that represent the upstream signaling events, trafficking of AMPAR to and from the PSD, lateral diffusion in the plane of the spine membrane, and the presence of an extrasynaptic AMPAR pool. Using idealized and realistic spine geometries, we show that the dynamics and increase of bound AMPAR at the PSD depends on a combination of endo- and exocytosis, membrane diffusion, availability of free AMPAR, and intracellular signaling interactions. We also found non-monotonic relationships between spine volume and change in AMPAR at the PSD, suggesting that spines restrict changes in AMPAR to optimize resources and prevent runaway potentiation.