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，已报道精神分裂症患者脑中的复合蛋白II减少。因此，复合蛋白II可能是导致精神分裂症发病的作用因子之一。研究了复合蛋白II基因缺陷小鼠的生理特性及其对母体剥夺应激的易感性。作为应激模型，我们采用了母亲剥夺应激，其中幼仔出生后2至16天与母亲分开，每天1小时。本实验观察了应激小鼠的生理特性和行为学变化。采用脑片制备方法，用电生理技术测定了小鼠海马CA1区的场兴奋性突触后电位。Morris水迷宫测试大鼠空间记忆能力。结果总结如下。敲除小鼠未显示任何特定的表型。在应激环境下繁殖的野生型小鼠也 ...更多信息 未显示异常。另一方面，暴露于母性剥夺应激的基因敲除小鼠表现出如下异常。（1）基本传递与野生型小鼠无差异。（2）高频电刺激诱发的强直后增强（post-tetanic potentiation）在基因敲除小鼠中明显减弱。（3）在应激敲除小鼠中，CNS中代表性的突触可塑性，即长时程增强，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功能部分受到抑制。（5）应激小鼠的运动学习电位无异常，说明（1）复合蛋白II基因敲除小鼠的形态学特征和生理特性均无异常。（2）母体剥夺应激影响了基因敲除小鼠以海马为关键的脑功能，如突触可塑性和空间记忆，而野生型小鼠则没有影响。（3）运动学习功能不受影响，小脑在运动学习中起重要作用。我们的研究结果表明，复杂蛋白II基因敲除小鼠揭示了脆弱性，在他们的发展过程中，母亲剥夺的压力。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