Maternal depression presents risks to both fetal and child development. While treating maternal depression with antidepressants during pregnancy can alleviate the condition, it also has implications for the development of the offspring. Our study aims to explore the impact of maternal depression and/or prenatal antidepressant treatment on offspring neuronal excitability.We implemented an animal model of maternal depression through chronic and unpredictable stress exposure. Mirtazapine served as the chosen antidepressant. Four experimental groups were used: no stress with vehicle, stress with vehicle, no stress with mirtazapine, and stress with mirtazapine. Primary hippocampal cultures were established from the pups' brains at the day of birth. Acute hippocampal slices were obtained between postnatal days 11 and 13. Whole cell patch clamp was employed to evaluate alterations in the excitability.Within the hippocampal neurons of both primary cultures and acute slices, we monitored passive membrane parameters, characteristics related to the generation of action potentials (AP), a series of APs, and spontaneous activity. In primary cultures, stress had a significant impact on the resting membrane potential (Vrest). Furthermore, in both slices and cultures, stress alone or in conjunction with mirtazapine induced significant changes in most of individual AP and AP series parameters. The occurrence of spontaneous activity was exclusive to acute slices. Despite variations across experimental groups, there were no significant changes observed in the average number of fired APs in hippocampal neurons.To conclude, maternal stress and mirtazapine treatment collectively influenced the excitability of hippocampal neurons in the offspring.