Prenatal maternal stress (PMS) is a major public health concern with long-lasting detrimental effects on maternal and offspring health. Supportive social relationships can buffer these effects, yet the underlying molecular mechanisms remain poorly understood. We previously showed that prosocial behaviors from a conspecific toward PMS-exposed females improve offspring recognition memory and social interaction, particularly in females. Here, pregnant mice were exposed to unpredictable stressors and then housed (ESA) or not housed (ES) with a familiar non-pregnant female until delivery. A non-stressed, socially housed group (CTA) served as control. PMS induced fragmented, low-quality maternal care (ES vs. CTA), fully restored in ESA. Performance in the 4-hole board test showed reduced exploration and impaired spatial memory in ES females compared to CTA and ESA females. ES dams exhibited lower Npas4 expression in the amygdala and reduced Comt1 in the prefrontal cortex and amygdala compared with CTA and ESA. Female offspring of ES dams showed decreased expression of Bdnf, Trkb, Npas4, and synapsin relative to CTA, whereas ESA offspring displayed full recovery of these gene expression. These results confirm previously observed memory deficits and suggest their association with sex-specific downregulation of genes involved in neuronal activity, synaptic plasticity, and memory formation, and that social support during pregnancy can reverse both behavioral and molecular alterations