Developmental plasticity shapes synaptic phenotypes of autism-associated neuroligin-3 mutations in the calyx of Held.

Abstract excerpt

Neuroligins are postsynaptic cell-adhesion molecules that bind to presynaptic neurexins. Mutations in neuroligin-3 predispose to autism, but how such mutations affect synaptic function remains incompletely understood. Here we systematically examined the effect of three autism-associated mutations, the neuroligin-3 knockout, the R451C knockin, and the R704C knockin, on synaptic transmission in the calyx of Held, a...

Topics

• Animals
• Autistic Disorder
• Cell Adhesion Molecules, Neuronal
• Disease Models, Animal
• Gene Knock-In Techniques
• Hippocampus
• Membrane Proteins
• Mice
• Mice, Knockout
• Mutation
• Nerve Tissue Proteins
• Neuronal Plasticity
• Neurons
• Synapses