This study employs mathematical modeling to investigate the spatial and temporal dynamics of intracellular Ca²⁺ signaling in cerebellar granule cells (GrCs), focusing on the regulation of Ca²⁺ gradients by endogenous buffers, mitochondrial transport, and endoplasmic reticulum (ER) release. Simulations were performed to assess the effects of calretinin, a key Ca²⁺ buffer, on Ca²⁺ diffusion, decay kinetics, and local concentration changes. The results demonstrate that calretinin significantly reduces the free Ca²⁺ concentration near open NMDA receptor channels and accelerates Ca²⁺ clearance after channel closure. Additionally, IP₃-mediated Ca²⁺ release from the ER modestly enhances the amplitude of Ca²⁺ transients, while mitochondrial uptake contributes to Ca²⁺ buffering but does not significantly alter peak amplitudes. The findings suggest that the spatial organization of Ca²⁺ handling systems plays a crucial role in shaping synaptic and action potential-induced Ca²⁺ signals, which are essential for synaptic plasticity and signal integration in GrCs.