Neuroligins and neurexins are molecules that bridge the gaps between one neuron and another at synapses in the brains of humans and other animals. Recent human clinical genetics studies have revealed mutations in the genes that code for neuroligins and neurexins in some patients with autism spectrum disorders. These mutations alter the function of these synaptic bridge molecules and thereby alter the function of synapses. This leads to abnormally altered communication between neurons in neuronal circuits of the brain. When these mutations in the human genes are reproduced in mice, the mice show abnormal social behaviors and other behaviors relevant to human autism. Using these genetic animal models, neuroscientists are now in a position to decipher the precise functional abnormalities in the brain that result from these autism-associated genetic mutations. Ongoing studies are using recordings from brain slices in these mouse models to understand the exact problems with brain function and to identify drugs or other treatments that can be used to normalize the function of brain synapses and circuits. Efforts to use this information to treat behavioral abnormalities in mouse models and ultimately in patients with autism are underway.