The developing neocortex exhibits spontaneous network activity with various synchrony levels, and such activity is selectively required during a critical developmental time window for the formation of long-range axonal projections connecting the two cortical hemispheres.

A simple mechanism, based on the synergy of two major opposing voltage-dependent currents that are ubiquitous in neurons, produces functional diversity of developing Renshaw cells in the embryo.

A mechanistic model based on the interaction of activity-independent cues from potential synaptic partners and local activity-dependent synaptic plasticity generates growing dendritic morphologies and non-random synaptic organization during development.

RNA sequencing and genetic mouse models reveal that transcriptional changes to astrocytes in the developing cortex are not intrinsic but influenced by their environment and determine that expression of astrocyte synapse-regulating genes and neuronal synaptogenesis is modulated by ongoing astrocyte-neuron communication.

Different Purkinje cell subpopulations show distinct developmental profiles of physiological activity, climbing fiber inputs and axonal and dendritic morphology, matching different timelines of cerebellum-dependent behaviors.

RNA sequencing and conditional Nova mutants reveal that Nova protein function is necessary for activity-dependent alternative splicing of synaptic genes within somatostatin cortical interneurons and regulates its afferent and efferent connectivity.

Following fertilization, the pioneering transcription factors GAGA factor (GAF) and Zelda are independently required to reprogram the zygotic genome of Drosophila and activate the first wave of gene expression.

Activity-dependent neurite outgrowth and neuronal migration interact to shape modular mesoscale network architecture by homeostatic self-organization.

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

Oligodendrocytes are actively engaged in the precise control of synaptic functions in the CNS through activity-dependent BDNF signaling.