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

两次打击假说被称为精神分裂症发病机制的假说。它假设精神分裂症的发病最初归因于大脑的脆弱性，这源于遗传或早期发育因素，而暴露于后来获得的因素，如压力，触发了发病。本研究探讨是否有新生大鼠重复治疗的NMDA拮抗剂（MK-801），精神分裂症的动物模型之一，有应激脆弱性。重复给予新生MK-801的大鼠在成年期接受20天（5天/周× 4周）强迫游泳应激。在此之后，进行了行为测试。这些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.