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Objective Early exposure to enriched environment may deeply influence the developing synaptic plasticity and this effect can transmit to offspring.Prolonged febrile seizures (FSs) are associated with a risk of subsequent temporal lobe epilepsy.In this study, we tested whether this acquired enhancement of susceptibility can be transmitted to offspring, and what is the risk factor during this transmission.Methods Prolonged seizures were evoked by exposing rat pup (~P9) to a hyperthermic environment of (44±2) ℃.Kainic acid, pentylenetetrazol (PTZ) and maximal electroshock (MES) were used to test the seizure susceptibility in rats that experienced FSs (F0) and the susceptibility of seizures in the following 2 generations (F1, F2) was tested as well.FSs mothers were mated with non-FSs fathers and vice versa to reveal which parent contributed to the transmissional phenomenon.Results (i) Both MES and kainic acid induced higher scores of seizures in the F1-FSs rats, while there is no significant difference in PTZ induced seizures compared with those of control rats.(ii) There was no significant difference in scores of MES-induced epilepsy between the F2 control and FSs groups.(iii) Offspring of F0 rats that had experienced 10 FSs displayed higher scores to MES-induced seizures than that of offspring in control group and 4*2 FSs group; however, offspring of F0 rats that had experienced 4*2 FSs did not display significant difference to MES-induced seizures.(iv) Scores of MES-induced seizures in F1 rats mated by FSs mother and non-FSs father are higher than that by FSs father and non-FSs mother.Conclusion These results indicate that (1) the transgenerational transmission showed severity-dependent and model-dependent characteristics; and (2) the transgenerational transmission was limited to F1 generation through the mother.Our finding may suggest non-Mendelian transgenerational inheritance play a role in the epileptogenesis.