Analysis of the synapse function in Neuroligin knock-in mice generated as models of autism.

为了研究自闭症的发病机制，我们分析了神经素-3 R451C突变小鼠模型的突触功能。我们发现由NMDA谷氨酸受体介导的突触传递在这些小鼠海马中增强，这是由于突触膜上受体数量的增加。此外，我们还发现突变突触的形态学异常。这些发现可能为理解自闭症的病理生理学和开发治疗方法提供见解。

To study the pathogenesis of autism, we analyzed the synaptic function in mouse models harboring Neuroligin-3 R451C mutation. We found that the synaptic transmission mediated by NMDA glutamate receptors was enhanced in the hippocampus of these mice and this was due to the increased number of the receptor on the synaptic membrane. In addition, we found morphological abnormalities in the mutant synapses. These findings may provide insight into understanding the pathopysiology and developing treatments of autism.