Olfactory receptor neuron (ORN) axons form the olfactory nerve (ON) and project to the glomerular layer of the olfactory bulb where they form excitatory synapses with terminal arborisations of the mitral cell (MC) tufted primary dendrite. Clusters of MC dendritic tufts define olfactory glomeruli where they involve in complex synaptic interactions. The computational function of these cellular interactions is not clear. We used patch-clamp electrophysiology combined with whole field or two-photon calcium imaging to study ON stimulation-induced Ca²⁺ signaling at the level of individual terminal branches of the MC primary dendrite in mice. ON-evoked subthreshold EPSPs induced Ca²⁺ transients in the MC tuft dendrites that were spatially inhomogeneous, exhibiting discrete hot spots. In contrast, Ca²⁺ transients induced by backpropagating action potentials (bAPs) occurred throughout the dendritic tuft, being larger in the thin terminal dendrites than in the base of the tuft. Single ON stimulation-induced calcium transients were depressed by the NMDA receptor antagonist D-aminophosphonovaleric acid (D-APV), increased with increasing stimulation intensity, and typically showed a prolonged rising phase. The synaptically induced calcium signals reflect, at least in part, dendro-dendritic interactions that support intraglomerular coupling of MCs and generation of an output that is common to all MCs associated with one glomerulus.