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.

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 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.

A novel algorithm, consensus non-negative matrix factorization (cNMF), accurately identifies gene expression programs underlying cell-type identity and cellular activities from single-cell RNA-Seq data.

Spines with multiple excitatory contacts are potential sites for competition between thalamic and cortical axons, which is regulated by the astrocytes through the secreted synaptogenic protein hevin.