Are rats with neonatal repeated treatment of an NMDA antagonist, an animal model for schizophrenia, vulnerable to stress?

双重打击假说是精神分裂症发病机制的一种假说。它假设精神分裂症的发病最初归因于遗传或早期发育因素导致的大脑脆弱性，而暴露于后来获得的因素（如压力）会引发发病。本研究考察了新生期反复服用NMDA拮抗剂（MK-801）（精神分裂症的动物模型之一）的大鼠是否具有应激易感性。在成年期，给予新生儿MK-801重复治疗的大鼠进行20天（5天/周x 4周）的强迫游泳应激。之后，进行了行为测试。研究结果并不表明这些动物具有压力脆弱性。

The two-hit hypothesis is known as a hypothesis of onset mechanism of schizophrenia. It assumes that the onset of schizophrenia is originally attributed to vulnerability of a brain which stems from genetic or early developmental factors, and that exposure to later acquired factors such as stress triggers the onset. The present study examined whether rats with neonatal repeated treatment of an NMDA antagonist (MK-801), one of the animal models for schizophrenia, have stress-vulnerability. Rats with repeated neonatal MK-801 treatment were subjected to 20-day (5 days/week x 4 weeks) forced-swim stress in adulthood. After that, behavioral tests were carried out. The results do not show that these animals have stress-vulnerability.