Cover Story：Activity-dependent synaptic structural plasticity underlies the learning and memory. Mammals, especially the rodents, are very sensitive to odorants, and have considerable capability of odor learning and memory. Here, the activity-dependent synaptic structural plasticity in the olfactory bulb (OB) of the CNGA2 knock-out transgenic mice (CNGA2 KO), which is anosmic, was investigated. Using immunohistochemistry for specific presynaptic and postsynaptic markers, it was found that deficits of peripheral inputs induced significant decreases in the expression of synaptophysin, a general marker for synapses, and gephyrin, a marker for inhibitory synapses, in the external plexiform layer (EPL) and the granule cell layer (GCL), but the vesicular glutamate transporters 1 (VGluT1) decreased only in EPL, not in GCL. Western-blots showed the decreases in the expression of gephyrin in the OB of CNGA2 KO mice, but not in the expression of the VGluT1. The results of immunohistochemistry and Western blot revealed that the excitatory and inhibitory synapses may have changed after deficits of peripheral inputs. GCs were the main participants in the EPL and GCL in the OB. Dendritic spines are the postsynaptic sites of the majority of excitatory synapses in the mammalian central nervous system, and the morphology and dynamics of dendritic spines change in response to novel experiences and neuropathologies. In the OB, spines on mature GCs are recipients of glutamatergic synapses in the GCL and reciprocal synapses in the EPL. Almost all study related to structural plasticity of GCs concentrated on the adult-born GCs, but the number of new-born granule cells in the OB is negligible compared with the number of preexisting GCs.