Interestingly, some epidemiological studies suggest that exposure to ionizing radiation may be a risk factor for Sarafloxacin HCl schizophrenia in adult humans. On the next day, after rats were trained for 5 days with four trials per day, the platform was moved to the opposite quadrant. A probe trial was carried out after four trials identical to the training sessions. The platform was removed and rats were allowed to swim freely for 60 sec. The time spent in the quadrant where the platform has been previously located was used as an index of spatial reference memory. The major findings of the present study are that fractionated ionizing irradiation to the adult male rat brain causes schizophrenia-relevant abnormal behaviors at three months after the irradiation. To the best of our knowledge, this is the first report demonstrating an animal model of schizophrenia by irradiation at adulthood. Picroside-II Although the irradiated adult rats may show essential features relevant to schizophrenia, the pathophysiological mechanism underlying these behavioral changes remains unclear. A recent study using postmortem brain samples demonstrated that proliferation of hippocampal neural stem sells was significantly reduced in patients with schizophrenia, but not unipolar depression, suggesting that reduced neural stem cell proliferation may contribute to the pathogenesis of schizophrenia. Moreover, it has been reported that the reduction of cell proliferation in the SGZ after repeated administration of the NMDA receptor antagonist phencyclidine may occur in tandem with PCP-induced behavioral changes in rats. In this regard, it is likely that reduction of adult neurogenesis by irradiation may be involved in the schizophrenia-like behavioral abnormalities in rats. Recently, the association between neurogenesis dysfunction and schizophrenia has been also demonstrated. Monje et al. observed that irradiation of the brains of adult rats produced neural progenitor cell dysfunction within the neurogenic zones of the hippocampus, regions plausibly implicated in cognitive deficits. Furthermore, it has been suggested that irradiation-induced cognitive deficits in animals may be associated with a decrease in hippocampal proliferation and a decrease in adult neurogenesis.