One of the risk factors for schizophrenia is maternal infection. We have previously shown that Polyriboinosinic-polyribocytidylic acid (poly I:C) induced maternal immune activation in mice caused histological changes in the hippocampal CA1 area of offspring during the developmental period and impaired sensorimotor gating in offspring during adulthood, resulting in behavioral changes. However, it remains unclear how maternal immune activation functionally impacts the hippocampal neuronal activity of offspring. We studied the effect of prenatal poly I:C treatment on synaptic transmission of hippocampal CA1 pyramidal cells in postnatal and adult offspring. Treatment with poly I:C diminished excitatory and enhanced inhibitory (GABAergic) synaptic transmission on pyramidal cells in adult offspring. During the early developmental period, we still observed that treatment with poly I:C decreased excitatory synaptic transmission and potentially increased GABAergic synaptic transmission, which was uncovered under a condition of high extracellular potassium-activated neurons. In conclusion, we demonstrate that maternal immune activation decreased excitatory and increased inhibitory synaptic transmission on hippocampal pyramidal cells from an early developmental period to adulthood, which could result in net inhibition in conjunction with poor functional organization and integration of hippocampal circuits.

精神分裂症的危险因素之一是母体感染。我们之前的研究表明，多聚核糖肌苷-聚核糖胞苷酸（poly I:C）诱导小鼠母体免疫激活，导致发育期后代海马 CA1 区组织学变化，并在成年期损害后代感觉运动门控，导致行为改变。然而，目前尚不清楚母体免疫激活如何在功能上影响后代的海马神经元活动。我们研究了产前 Poly I:C 治疗对产后和成年后代海马 CA1 锥体细胞突触传递的影响。 Poly I:C 治疗可减少成年后代锥体细胞的兴奋性和增强抑制性（GABA 能）突触传递。在发育早期，我们仍然观察到，聚 I:C 治疗会减少兴奋性突触传递，并可能增加 GABA 能突触传递，这是在高细胞外钾激活神经元的条件下发现的。总之，我们证明，从早期发育期到成年期，母体免疫激活降低了海马锥体细胞的兴奋性并增加了抑制性突触传递，这可能导致净抑制以及海马回路功能组织和整合不良。