Mice that lack the autism susceptibility gene Semaphorin 5A show excess excitatory synapse formation in dentate granule neurons and also altered social behavior, adding to evidence that a surplus of synapses contributes to the behavioral changes observed in autism spectrum disorders.

Protein kinase A regulates the rapid, activity-dependent genesis of excitatory synapses during striatal development.

The secretory and recycling components of neuronal dendrites, smooth endoplasmic reticulum and endosomes, were discovered to support synaptogenesis underlying a cellular mechanism of learning and memory in the developing brain.

Brain-derived neurotrophic factor (BDNF)/TrkB.T1 signaling contributes to astrocyte morphological maturation, with implications for neuronal synaptogenesis and function and astrocyte functional maturation.

Modelling O-GlcNAc transferase intellectual disability reveals the roles of this post-translational modification in regulating normal axonal terminal morphology and maintaining appropriate sleep homeostasis, pharmacological and genetic rescues of O-GlcNAcylation highlight the complexities of addressing this disorder.

Overexpression of the growth factor neurotrophin-3 helps to repair noise-induced damage in the mouse inner ear by promoting the regeneration of damaged synapses.

Genetic studies in mice identify the transcription factor MafB as a potent regulator of specific features of the synapses underlying hearing.

A novel molecular mechanism linking a neurotrophin with a Toll-family and kinase-less Trk-like receptors provides a direct link from molecules to structural circuit plasticity and modification of behaviour.

A protein that is a building block of intercellular bridges between neurons promotes their ability to grow dendrites and make synapses.

Axonal arborisation growth is regulated by dynamic, focal localisations of Neurexin and Neuroligin that provide stability for filopodia, enabling a 'stick and grow'-based mechanism, wholly independent of synapse formation.