Stanford Neurosciences Institute Seminar Series Presents
Neuroligins in inhibitory synaptic signaling - from synapse formation to autism spectrum disorders
Nils Brose, Ph.D
Director and Professor of Experimental Medicine, Max-Plank Institute
Host: Lu Chen
Abstract
Presenting biochemical, structural biology, cell biological, and electrophysiological data demonstrating that Neuroligin-2 and Neuroligin-4 regulate the recruitment of GABAA-receptors to nascent inhibitory synapses by activating the signaling/scaffold protein Collybistin. The main functional defects resulting from Neuroligin-4 loss in mice are subtle reductions in GABAA-receptor signaling in several brain regions, such as the CA3 region of the hippocampus, which lead to promient changes in oscillatory network activity. These data indicate that defects in GABAergic signaling and the consequent changes in network activity are causally involved in the autism-like behavioral defects seen upon Neuroligin-4 mutation.
