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首页> 外文期刊>The European Journal of Neuroscience >Abnormalities of presynaptic protein CDCrel-1 in striatum of rats reared in social isolation: relevance to neural connectivity in schizophrenia.
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Abnormalities of presynaptic protein CDCrel-1 in striatum of rats reared in social isolation: relevance to neural connectivity in schizophrenia.

机译：社交隔离饲养的大鼠纹状体中突触前蛋白CDCrel-1异常：与精神分裂症的神经连通性有关。

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Abstract Post-weaning social isolation-rearing of rats leads to behavioural and neurochemical sequelae that model aspects of schizophrenia, and it may be useful to test hypotheses related to putative molecular mechanisms of the illness. In humans, the presynaptic protein CDCrel-1 represents an interesting candidate molecule for the mechanism and aetiology of schizophrenia. CDCrel-1 modulates dopamine neurotransmission, binds to the SNARE protein syntaxin and maps onto a region of chromosome 22q11 deleted in velo-cardio-facial and DiGeorge syndromes, which are associated with increased prevalence of schizophrenia. Using the isolation-rearing model, we measured immunoreactivity of the synaptic proteins CDCrel-1, synaptophysin and syntaxin. Male, Sprague-Dawley rats were raised in groups or in isolation for 12 weeks from weaning. Synaptic protein immunoreactivities were measured in striatal and hippocampal homogenates, using a sensitive enzyme-linked immunoadsorbent assay with monoclonal antibodies. Isolation-rearing produced region- and protein-specific effects. CDCrel-1 immunoreactivity was significantly lower in the striatum and marginally higher in the hippocampus of isolation-reared compared with socially reared animals. There were no statistically significant differences in synaptophysin immunoreactivity in either region. Confocal microscopy demonstrated a high degree of colocalization between the two presynaptic proteins. In striatum, a robust relationship between CDCrel-1 and syntaxin immunoreactivities was observed in socially reared rats, this was lost in the isolation-reared animals. Altered levels of the septin CDCrel-1 in isolation-reared rats may contribute to changes in neuronal connectivity and neurotransmission, and suggest a potential role for CDCrel-1 in schizophrenia related to chromosome 22q11 deletion syndrome.
机译：摘要断奶后大鼠社会隔离的抚养导致行为和神经化学后遗症，对精神分裂症的各个方面进行建模，可能有助于检验与该疾病的推测分子机制有关的假设。在人类中，突触前蛋白CDCrel-1代表了精神分裂症的机制和病因的有趣候选分子。 CDCrel-1调节多巴胺神经传递，与SNARE蛋白语法结合，并定位到22心率染色体上的区域，该区域在心肺面部综合征和DiGeorge综合征中缺失，这与精神分裂症的患病率增加有关。使用分离饲养模型，我们测量了突触蛋白CDCrel-1，突触素和语法素的免疫反应性。从断奶开始，成组或单独饲养雄性Sprague-Dawley大鼠12周。使用敏感的酶联免疫吸附法和单克隆抗体，在纹状体和海马匀浆中测量突触蛋白的免疫反应性。分离育种产生了区域和蛋白质特异性效应。与社交饲养的动物相比，隔离饲养的海马中的CDCrel-1免疫反应性显着降低，海马中的CDCrel-1免疫反应性显着升高。任一区域的突触素免疫反应性均无统计学上的显着差异。共聚焦显微镜显示两种突触前蛋白之间高度共定位。在纹状体中，在社交饲养的大鼠中观察到了CDCrel-1和Syntaxin免疫反应性之间的牢固关系，而在隔离饲养的动物中这种关系消失了。隔离饲养的大鼠中Septin CDCrel-1水平的改变可能有助于神经元连接性和神经传递的变化，并暗示CDCrel-1在与22q11号染色体缺失综合征相关的精神分裂症中的潜在作用。

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