Neuronal plasticity is a fundamental property of the nervous system that allows a change in the response to stimulation by reorganizing its structure, functions and connections. Among the main regulators of neuronal plasticity are perineuronal nets (PNNs), condensed forms of extracellular matrix (ECM) that enwrap mainly parvalbumin expressing (PV+) inhibitory interneurons. Glycoprotein tenascin-C (TnC) is one of the ECM molecules that interacts with components of PNNs and that modulates the synaptic plasticity in the hippocampus. The aim of this study was to investigate whether TnC deficiency affects the number, intensity and structure of PNNs around PV+ and PV- cells, the ultrastructure of PNNs, as well as the expression of inhibitory and excitatory synaptic terminals (puncta) penetrating the PNN mesh in the hippocampus. In order to enhance neuronal plasticity, TnC-deficient (TnC-/-) and wild-type (TnC+/+) young adult male mice were reared in an enriched environment and in control standard environment (EE and SE) for 8 weeks. The most pronounced alterations in the expression of PNNs and synaptic markers occurred in the dentate gyrus (DG) and CA2 hipocampal regions. TnC deficiency and EE had no significant effect on the number and intensity of PNNs, on the number of PV neurons or on the synaptic expression in the CA1 region. In conclusion, our findings indicate that TnC is involved in modulating structural plasticity of the hippocampus, especially in DG and CA2 regions which emerged as focal points of alterations in perineuronal nets and synaptic terminals due to TnC deficiency and environmental enrichment.