Browning M D, Dudek E M, Rapier J L, Leonard S, Freedman R
Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.
Biol Psychiatry. 1993 Oct 15;34(8):529-35. doi: 10.1016/0006-3223(93)90195-j.
The levels of the synaptic vesicle-associated proteins, synapsin and synaptophysin, were examined in human postmortem hippocampus from the brains of schizophrenics and age-matched controls using a quantitative western blot analysis. The schizophrenic samples had significantly lower levels of synapsin I than controls. In individual data, five of the seven schizophrenic samples had extremely low levels of synapsin, whereas two of the schizophrenic samples had normal levels of synapsin. This deficit in synapsin does not appear to be due to some non-specific neuronal loss as the levels of the other synaptic vesicle marker, synaptophysin, were near normal in all seven schizophrenics. Given that synapsin is thought to regulate neurotransmitter release, it is possible that this deficit in synapsin could result in abnormal processing of neuronal information as is seen in various sensory processing abnormalities associated with schizophrenia.
利用定量蛋白质免疫印迹分析，检测了精神分裂症患者及年龄匹配的对照者死后大脑海马体中突触囊泡相关蛋白——突触结合蛋白和突触素的水平。精神分裂症患者样本中突触素I的水平显著低于对照组。在个体数据中，7个精神分裂症样本中有5个的突触素水平极低，而另外2个精神分裂症样本的突触素水平正常。突触素的这种缺乏似乎并非由于某些非特异性神经元丢失，因为在所有7名精神分裂症患者中，另一种突触囊泡标记物——突触囊泡蛋白的水平接近正常。鉴于突触素被认为可调节神经递质释放，突触素的这种缺乏可能会导致神经元信息处理异常，就像在与精神分裂症相关的各种感觉处理异常中所见到的那样。
