Molecular Mechanisms

The neurexin ligands, neuroligins and leucine-rich repeat transmembrane proteins, perform convergent and divergent synaptic functions in vivo.

Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia.

Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function.

An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus.

Mechanisms of inhibition within the telencephalon: “where the wild things are.”

Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons.

Neurobiology meets genomic science: The promise of human-induced pluripotent stem cells.

Axon selection: from a polarized cytoplasm to a migrating neuron.

Mutations causing syndromic autism define an axis of synaptic pathophysiology.

Activity-dependent phosphorylation of GABA A receptors regulates receptor insertion and tonic current.

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