The possible animal model for schizophrenia by targeting the protein that was reported to be decreased in the expression in the brain of schizophrenic patient by postmortem study

根据尸检研究发现，精神分裂症患者脑内复合素II含量降低，因此可以认为复合素II可能是导致精神分裂症发病的因素之一。我们研究了复杂蛋白II基因缺陷小鼠的生理特征及其对母体剥夺应激的易感性。作为应激模型，我们采用了母体剥夺应激，即仔鼠在出生后2-16天与母亲分离，每天1小时。我们检测了应激小鼠的生理特性和行为。采用电生理技术，采用脑片法制备场兴奋性突触后电位，测定小鼠海马CA1区场兴奋性突触后电位。用Morris水迷宫测试大鼠的空间记忆能力。研究结果总结如下。基因敲除的小鼠没有表现出任何特殊的表型。在应激环境下培育的野生型小鼠也有…更多的人没有表现出异常。另一方面，暴露在母体剥夺应激下的基因敲除小鼠表现出如下异常。(1)基本传播与野生型小鼠无差异。(2)在基因敲除小鼠中，高频电刺激引起的短时可塑性之一--强直性后增强显著降低。(3)应激基因敲除小鼠中枢神经系统中具有代表性的突触可塑性--长时程增强被消除，而长时程抑制没有改变。(4)应激基因敲除小鼠的空间记忆部分受到抑制。(5)应激小鼠的运动学习电位未见异常。结论：(1)复合蛋白II基因敲除小鼠在形态特征和生理特性上均未出现异常。(2)母系剥夺应激对突触可塑性、空间记忆等脑功能有重要影响，而野生型小鼠无明显变化。(3)对小脑起重要作用的运动学习无影响。我们的结果表明，复杂蛋白II基因敲除小鼠在发育过程中对母体剥夺压力表现出脆弱性。较少

Complexin II has been reported to be decreased in the brain of schizophrenic patient according to the postmortem study., therefore complexin II could be assumed as the one of actors which contributes the onset of schizophrenia. We investigated the physiological characters of complexin II gene deficient mouse and its vulnerability to the maternal deprivation stress. As a stress model, we adopted the maternal deprivation stress in which the pups were separated from their mother between 2 and 16 day after birth fur one hour every day. We examined the physiological property and behavior of stressed mice. Field excitatory postsynaptic potential was measured with electrophysiological technique in the CA1 area of mouse hippocampus using brain slice preparation. Their spatial memory was examined by Morris Water maze test. The results are summarized as the following. The knockout mouse did not show any particular phenotype. The wild-type mice that were bred under the stressed circumstance also … More did not show abnormality. On the other hand, the knockout mouse that was exposed to the maternal deprivation stress showed the abnormality as the followings. (1)The basic transmission was not differed from that of wild-type mouse. (2)Post-tetanic potentiation, one of the short-term plasticity, which was induced by high frequency electrical stimulation, was significantly decreased in the knockout mouse. (3)The representative synaptic plasticity in the CNS, long-term potentiation, was eliminated in the stressed knockout mouse, whereas long-term depression was not altered. (4)The spatial memory was partially suppressed in the stressed knockout mouse. (5)There was no abnormality in the potential of motor leaning in the stressed mouse.We concluded that (1)complexin II knockout mouse did not show abnormality in their morphological character and their physiological properties. (2)The maternal deprivation stress affected the brain function in which hippocampus plays a critical role, such as synaptic plasticity and spatial memory, of knockout mouse, whereas, not of the wild-type mouse. (3)The motor learning, in which the cerebellum plays an important role, was not affected. Our results suggest that the complexin II knockout mouse reveals vulnerability during their development to the maternal deprivation stress. Less