接触蛋白5(CNTN5)属免疫球蛋白超家族成员,高度表达于人脑的杏仁核区及枕叶区,在听觉系统的谷氨酸能神经元突触前末端表达丰富。近几年,人们通过动物实验以及免疫荧光实验发现CNTN5的生物学功能以及其与自闭症、阿尔兹海默症、神经性厌食症等精神障碍相关性疾病的联系。另外免疫荧光实验发现,CNTN5在下丘脑中只表达于谷氨酸能神经元,谷氨酸能神经元减少可导致突触的长时程增强,而长时程增强又是创伤后应激障碍(PTSD)的重要机制,这提示CNTN5基因突变是PTSD发生的机制之一。本文总结了CNTN5的研究进展,旨在找到CNTN5的未来研究方向。
Contactin 5 (CNTN5) belongs to a subgroup of the immunoglobulin superfamily, k is highly expressed in the amygdala and occipital lobe of the human brain as well as in the presynaptic terminal of glutamatergic neurons in the auditory system. In recent years, researchers have used animal experiments to identify the biological functions of CNTN5. They have also investigated the relationship between CNTN5 and mental disorders including autism, Alzheimer's disease, and anorexia nervosa among others. Furthermore, immunofluoreseence assays have shown that CNTN5 is expressed in glutamatergie neurons in the hypothalamus. A reduction in the number of glutamatergie neurons can cause the long-term po- tentiation of synapses. Long-term potentiation is an important mechanism in post-traumatic stress disorder (PISD). It suggests that mutation of CNTN5 may be one of the mechanisms underlying PISD. We reviewed the research concerning CNTN5 to identify future research directions.