Long-term synaptic plasticity (LTP) is the fundamental cellular mechanism which underlies long-term storage of information in neuronal circuits. Synaptic plasticity has mainly been studied on excitatory pyramidal neurons during memory formation. However, GABAergic interneurons are key players in orchestrating the dynamic of excitatory neuronal networks during this process. Thus, the excitatory synapses onto interneurons are central to this control as they constrain pyramidal-cells activity and set synaptic plasticity at excitatory-excitatory synapses. Nonetheless, how, when and where plasticity at excitatory-interneurons synapses occurs during learning and memory remains to be elucidated. The aim of this study is to evaluate the role of AMPAr mobility in LTP at excitatory-interneurons synapses in the hippocampus. To do so, we use KI mice that express an AP-tag on the GluA1 subunit of AMPA receptors. Expression of the BiRA enzyme in hippocampal inhibitory interneurons in the CA1 region with an AAV construct under the control of the mDlx promoter (AAV-mDlx-BirA-eGFP) allows us to biotinylate the AP-tag. Then, exogenous application of neutravidin blocks the surface mobility of AMPA receptors which has already been shown by our lab to inhibit LTP on excitatory pyramidal cells in the hippocampus. By using this approach, we observed that blocking GluA1-containing AMPAr mobility on inhibitory interneurons impairs LTP at excitatory-interneurons synapses. Our results suggest that like excitatory pyramidal neurons in CA1, LTP on interneurons depends on AMPAr surface mobility. Taken together, these results pave the way to study the role of LTP on different inhibitory interneuron subclasses at key stages of memory formation.