The full-length amyloid precursor protein (APP), a key player in Alzheimer’s disease (AD), is ubiquitously expressed in a large majority of neurons, including GABAergic interneurons (INTs). Recent studies showed evidence of disrupted hippocampal plasticity in conditional APP KO of GABAergic forebrain neurons (Mehr et al, 2020). However, the physiological functions of APP at inhibitory synapses remain to be defined. We to study the role of APP at inhibitory synapses onto CA3 pyramidal cells (PCs) as well as on the overall inhibitory balance within the CA3 network. We combine slice electrophysiology and morphological analysis in order to highlight possible changes occurring at inhibitory synapses in the absence of APP. We first observed that selective deletion of APP and related APLP2 in CA3 INTs modified the properties of inhibitory currents in CA3 PCs, namely their amplitude and rise time. We then recorded intrinsic properties of CA3 INTs by current-clamp recordings, followed by imaging and morphological reconstruction. Based on a non-linear dimensionality reduction analysis, we were able to categorize recorded INTs into different clusters, possibly highlighting INTs subtypes. We observed no significant differences within clusters between control vs APP/APLPL2dKO cells. In order to investigate potential effects of the lack of APP/APLP2 in CA3 INTs on the global circuit activity and cell synchronicity, we are currently performing silicon probe in vivo recordings in CA3 in awake mice. Overall, our work will help to better understand the physiological contribution of APP on global neuronal activity and excitatory/inhibitory balance, impaired within hippocampal circuits in AD.