Disrupted balance between excitatory and inhibitory neuronal activity is considered a main driver of AD pathogenesis contributing to cognitive deficits. We studied the protein expression of GABAA- and glycine receptor subunits as well as the protein level and phosphorylation of the inhibitory receptor anchoring protein gephyrin in a mouse model of AD and how treatment with artemisinins modulates these features. In hippocampal subregions of 12-months-old double transgenic mice which co-express the Swedish mutated form of the human APP (APPswe) and at L166P mutated human presenilin 1 (PS1) genes (APP-PS1) artemisinins increased the protein levels of both gephyrin, and γ2-GABAA-receptor subunits which are otherwise all reduced in the hippocampus of APP/PS1 mice compared to age matched wild type animals. Similar changes were detected for protein levels and number of glycine receptor-alpha3 subunits. Whereas the increase of GABAA receptor protein in the hippocampus involved mainly synaptically localized receptors, as evidenced by confocal microscopy, in the case of glycine receptor alpha3 subunits predominantly the number of extrasynaptic localized receptors - thought to play a role in tonic inhibition- was elevated after treatment. Furthermore, we found, that the increased postsynaptic g2-GABAAR subunit density coincide with an increased phosphorylation of gephyrin at S270 through the serine kinase cyclin kinase 5 (CDK5), both of which are increased in the 3-months-old mouse hippocampus upon artemisinin treatment. Thus, our studies reveal a dynamic state of different subcellular localizations of inhibitory synaptic proteins in the hippocampus of APP-PS1 mice that can be modulated by the plant derived compounds, artemisinins.