Objective To establish a rat model of hippocampal injury in schizophrenia， and to investigate the protein phosphorylation activity of protein kinase B（ PKB/Akt） and forkhead box Os（ FoxOs） protein in the model brain. Methods Healthy male Sprague-Dawley rats were randomly divided into two groups： the neonatal ventral hippocampus lesion（ NVHL） and the control group， with 8 rats in each group. The model of NVHL was established by stereotactic injection with ibotenic acid. At 56-60 days， the rats were subjected to spontaneous activity， pre pulse inhibition（ PPI） and other behavioral tests. Three days after the test， the brain tissue was taken for morphological observation. Akt/FoxOs phosphorylation levels in cortex and striatum were measured by Western blot. Rusults Compared with the control group， the ventral hippocampus of NVHL rats was significantly damaged. Amphetamine induced spontaneous exploration activity increased ［（1 014±72） times vs.（ 753±87） times， P ＜ 0.01］， PPI was impaired［ PP6：（ 5.04±3.24）% vs. （22.08±14.26）%， PP9：（ 11.26±5.24）% vs.（ 25.16±13.45）%， PP12：（ 8.17±10.45）% vs.（ 29.16±10.25）%， all P＜ 0.01］ in the NVHL group. The phosphorylation levels of Akt/FoxO1 in cerebral cortex and Akt/FoxO1/ FOXO3a in striatum were decreased（ P ＜ 0.05）. Conclusions Ventral hippocampal injury is a widely used animal model of schizophrenia. After hippocampal injury， Akt/FoxOs protein phosphorylation levels in cortex and striatum of rats decreased， which further indicated that this pathway was involved in the process of schizophrenia.