Early life stress (ELS) is one of the key risk factors in the development of mental health disorders, strongly impacting the limbic system. Kainate receptors and GluK1 specifically have been previously shown to be affected, and potentially mediate some of the effects of ELS on GABAergic interneurons. Aims: To study the effects of the ELS on the circuitry of the ventral hippocampus (vHPC) and assess the potential of GluK1 as a tool for phenotype rescue.Methods: Limited bedding and nesting model of ELS was used in WT and PV-Cre mice and validated using standard behavioral tests in adults. Electrophysiological recordings were performed in CA1 of vHPC in acute slices at P60-P80. Custom-made viral vectors (AAV/mDlx-Grik1) were injected into the vHPC to overexpress GluK1 in GABAergic interneurons. Results: Following ELS we observed a reduced expression of GluK1 in the hippocampus of both male and female mice. The spontaneous synaptic events in either PV+ or pyramidal cells were not significantly affected, however, we recorded gender-specific changes in the cells’ intrinsic excitability. Furthermore, exposure to ELS reduced LTP in CA1 of vHPC. The ELS-induced changes in PV+ interneurons were effectively normalized with overexpression of GluK1. Conclusions: In the vHPC of adult animals ELS produces gender-specific functional changes in PV+ neurons and pyramidal cells and attenuates synaptic plasticity. Some of these changes can be successfully reversed in vitro via overexpression of GluK1 in the interneurons. Thus kainate receptors appear as a potential target for the treatment of stress-induced neuropsychiatric disorders.