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

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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.