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.

Clarinet, a novel C. elegans active zone protein with homology to vertebrate Piccolo and Rim, uses its different isoforms for diverse functions, including synaptic vesicle clustering, vesicle release and synaptogenesis.

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.

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

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.

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.

Competition between neurons for postsynaptic ephrin-B3 controls distribution of a limited pool of synapses and defines a novel trans-synaptic mechanism enabling neurons to set the number of synapses they receive.

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.