Studies of impaired synaptic functions in autism model mice that express a mutant neuroligin

在这个研究项目中，我从电生理学的角度研究了突变小鼠的突触功能，这些突变小鼠具有在人类自闭症患者中发现的突触粘附分子神经素的单个氨基酸突变，以及神经素表达受RNA干扰抑制的野生型神经元。在体感觉皮层，单氨基酸突变和神经木质素的敲除导致兴奋性和抑制性突触输入之间的不平衡。此外，在敲入小鼠中，发现海马长期增强的后期阶段选择性受损。

In this research project, I studied the synaptic functions electrophysiologically in mutant mice that possess a single amino acid mutation of a synaptic adhesion molecule neuroligin that was found in human autism patients as well as in wild type neurons in which neuroligin expression was suppressed by RNA interference. In the somatosensory cortex, both single amino acid mutation and knock-down of neuroligin led to an imbalance between excitatory and inhibitory synaptic inputs. Moreover, it was found that the late phase of long-term potentiation in the hippocampus was selectively impaired in the knock-in mice.