It is widely believed that synaptic transmission in the hippocampus plays a crucial role in formation of contextual memories. Data obtained in our laboratory implies that PSD-95 (postsynaptic density protein 95)-dependent synaptic plasticity in dCA1 area is required for updating of contextual fear memory.To check how inactivation of dCA1 area affects contextual fear memory extinction, we stereotactically injected the adenoviral vectors (AAVs) encoding DREADD receptor hM4 [AAV2.1:hSyn_hM4_mCherry]. Next we trained mice in contextual fear conditioning (CFC). We found that chemogenetic inhibition of dCA1 impaired contextual fear memory extinction and redacted the levels of synaptic protein, PSD-95. To see whether PSD-95 in dCA1 affects the contextual fear memory we stereotactically injected the lentiviral vectors (LVs) encoding short hairpin RNA (shRNA) silencing PSD-95 expression [H1-shRNA_PSD95-Ub_GFP] in the dCA1 area of young adult male and female mice. Next, we trained mice in CFC and performed electrophysiological recordings in the dCA1 area to assess the functionality of synapses with PSD-95 depletion. Moreover, we tested mice in the IntelliCages system to study spatial choice and extinction of appetitive contextual memories in close-to-ecologic conditions. We found that local depletion of PSD-95 in dCA1 decreased synaptic transmission and impaired the contextual fear memory extinction, but not formation or recall. It also impaired ability to find a reward in a complex context at the initial stage of learning, but had no effect on place preference extinction. Together, our data indicates that PSD-95-dependent synaptic transmission in dCA1 is required for updating contextual memories.