Objective To observe the effects of different doses of methylazoxymethyl acetate （MAM） on sensorimotor gating in rats， and to explore the appropriate dose of MAM in inducing rat model of schizophrenic sensorimotor gating disorder. Methods Different doses of MAM （25 mg/kg， 20 mg/kg， 15 mg/kg） were used to treat perinatal rats to induce the development of nervous system in their offspring， and to establish a rat model of schizophrenic sensorimotor gating disorder. The feasibility of establishing rat model of schizophrenic sensorimotor gating disorder with different doses of MAM was evaluated by observing prepulse inhibition of the startle response （PPI）， P50 auditory-evoked potential suppression （AEP-P50） and hippocampus neuron apoptosis detecting by Caspase 3 staining. Results PPI can be inhibited by MAM in the dose ranging from 15 mg/kg to 25 mg/kg （P ＜ 0.05）. The difference between the middle and high dose of MAM group and the control group was statistically significant （P＜0.05）. There was a significant difference in the amplitude of startle reflex between the high-dose mam group and the control group， with an increase of 34.32% （P ＜ 0.05）. The values of S2/S1， S2 peak to peak and S1 peak to peak in high-dose MAM group were higher than those in control group， medium dose and low-dose MAM groups， and the differences were statistically significant （P ＜ 0.05）. Pearson correlation analysis showed that there was no significant correlation between PPI and AEP-P50. The apoptosis rate of hippocampal neurons in high-dose MAM group was higher than that in medium， low-dose MAM group and control group， and the difference was statistically significant （P＜ 0.05）. Conclusions MAM can induce changes in PPI and AEP-P50 in rats， and MAM （25 mg/kg） can be used as a model drug in animal models of sensorimotor gating disorder in schizophrenia.