Imai C, Sugai T, Iritani S, Niizato K, Nakamura R, Makifuchi T, Kakita A, Takahashi H, Nawa H
Molecular Neurobiology, Brain Research Institute, Niigata University, 951-8585, Niigata, Japan.
Neurosci Lett. 2001 Jun 15;305(3):185-8. doi: 10.1016/s0304-3940(01)01844-4.
The application of DNA array technology to schizophrenic studies enabled us to assess molecular features of this disease. The expression of synapsin II and N-ethylmaleimide-sensitive fusion protein (NSF) mRNAs is reported to decrease in the prefrontal cortex of these patients. We attempted to reproduce this result with two distinct approaches. With high quality samples, mRNA and protein levels for synapsin II and NSF were measured by real-time polymerase chain reaction and by immunoblotting. Both experiments led to the same conclusion: The expression of these presynaptic markers is not altered significantly in the prefrontal cortex of our schizophrenic samples, compared to that in control subjects. These observations suggest that the neurochemical impairments of synapses reported in schizophrenia are not evident for all presynaptic markers and needs to be re-evaluated at molecular levels.
将DNA阵列技术应用于精神分裂症研究,使我们能够评估这种疾病的分子特征。据报道,在这些患者的前额叶皮质中,突触素II和N - 乙基马来酰亚胺敏感融合蛋白(NSF)的mRNA表达会下降。我们试图用两种不同的方法重现这一结果。使用高质量样本,通过实时聚合酶链反应和免疫印迹法测量突触素II和NSF的mRNA和蛋白质水平。两项实验都得出了相同的结论:与对照组相比,我们的精神分裂症样本前额叶皮质中这些突触前标记物的表达没有显著改变。这些观察结果表明,精神分裂症中报道的突触神经化学损伤并非在所有突触前标记物中都明显,需要在分子水平上重新评估。